Triptolide regulates neutrophil function through the Hippo signaling pathway to alleviate rheumatoid arthritis disease progression.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammatory changes in the joints, the etiology of which is unclear. It is now well established that regulated cell death (RCD) and migration of neutrophils play an important role in the pathogenesis of RA. Tripterygium wilfordii Hook.f (TwHF) is a total saponin extracted from the root of Tripterygium wilfordii Hook.f, a plant of the family Wesleyanaceae, which has strong anti-inflammatory and immunomodulatory effects and has been used as a basic drug in the clinical treatment of RA. Despite the good efficacy of TwHF treatment, the mechanism of action of TwHF remains unclear. Several studies have demonstrated that the drug tripterygium glycosides, in which TwHF is the main ingredient, has achieved excellent efficacy in the clinical treatment of RA. Investigations have also found that TwHF can affect cellular RCD, cell migration, cell proliferation, and the apoptosis-related Hippo signaling pathway. In this study, we first analyzed the RCD and migration differences of neutrophils in patients with RA through network pharmacology and transcriptome analysis. Subsequently, we used electron microscopy, immunofluorescence, and other methods to identify the RCD phenotype of neutrophils. In collagen-induced arthritis (CIA) model, we demonstrated that Triptolide (the main active ingredient in TwHF) could alleviate the progression of arthritis by reducing the bone destruction and the infiltration of neutrophils. Furthermore, in vitro experiments showed that Triptolide induced neutrophil apoptosis, inhibited the formation of neutrophil extracellular traps (NETs), and impeded the neutrophil migration process in a Hippo pathway-dependent manner. Taken together, these findings indicate that Triptolide has potential for treating RA and provide theoretical support for the clinical application of TwHF, as a traditional Chinese medicine, in RA.

Glutathione peroxidase 4 restrains temporomandibular joint osteoarthritis progression by inhibiting ferroptosis.

There are few effective therapeutic strategies for temporomandibular joint osteoarthritis (TMJOA) due to the unclear pathology and mechanisms. We aimed to confirm the roles of GPX4 and ferroptosis in TMJOA progression. ELISA assay was hired to evaluate concentrations of ferroptosis-related markers. The qRT-PCR assay was hired to assess gene mRNA level. Western blot assay and immunohistochemistry were hired to verify the protein level. CCK-8 assay was hired to detect cell viability. Human fibroblast-like synoviocytes (FLSs) were cultured to confirm the effects of GPX4 and indicated inhibitors, and further verified the effects of GPX4 and ferroptosis inhibitors in TMJOA model rats. Markers of ferroptosis including 8-hidroxy-2-deoxyguanosine (8-OHdG) and iron were notably increased in TMJOA tissues and primary OA-FLSs. However, the activity of the antioxidant system including the glutathione peroxidase activity, glutathione (GSH) contents, and glutathione/oxidized glutathione (GSH/GSSG) ratio was notably inhibited in TMJOA tissues, and the primary OA-FLSs. Furthermore, the glutathione peroxidase 4 (GPX4) expression was down-regulated in TMJOA tissues and primary OA-FLSs. Animal and cell experiments have shown that ferroptosis inhibitors notably inhibited ferroptosis and promoted HLS survival as well as up-regulated GPX4 expression. Also, GPX4 knockdown promoted ferroptosis and GPX4 overexpression inhibited ferroptosis. GPX4 also positively regulated cell survival which was the opposite with ferroptosis. In conclusion, GPX4 and ferroptosis regulated the progression of TMJOA. Targeting ferroptosis might be an effective therapeutic strategy for TMJOA patients in the clinic.

Endothelial cell protein C receptor regulates neutrophil extracellular trap-mediated rheumatoid arthritis disease progression.

Endothelial cell protein C receptor (EPCR) is a 46 kDa transmembrane protein receptor, expressed in most immune cells (T cells, monocytes, dendritic cells, polymorphonuclear neutrophils [PMN]). EPCR reportedly plays a vital role in rheumatoid arthritis (RA). Our results confirmed that EPCR expression exists in the PMN of RA patients, and animal experiments demonstrated that down-regulation of EPCR expression affects disease progression in collagen-induced arthritis (CIA) mice. PMN is the immune cell type that first enters the site of inflammation in the early stages of inflammation. In the early stage of RA, PMN cells migrate into the joint cavity and function in the process of RA synovial inflammation, aggravating the bone destruction found in RA and mediating the progression of RA disease progression. We verified the differences in EPCR expression in PMN cells between RA and osteoarthritis (OA) patients by Western blot and then confirmed this difference in animals. We found that CIA mice treated with PMN-neutralizing antibody intervention had reduced disease performance. On this basis, EPCR was knocked down at the same time. The therapeutic effect of PMN-neutralizing antibody treatment was subsequently diminished. To explore the relationship between EPCR and PMN in RA, we used immunofluorescence to detect the expression of PMN-neutrophil extracellular traps (NETs) in RA patients and used EPCR neutralizing antibodies as an intervention. The results showed that the formation of PMN-NETs in RA patients increased. Finally, through in vitro intervention experiments involving EPCR and PMN transcriptome analysis of the peripheral blood of RA patients, we concluded that EPCR may regulate the formation of PMN-NETs in RA patients through the activated protein C (APC)-EPCR signaling pathway, thereby affecting the progression of disease in RA patients.

Phenotype and molecular characterizations of a family with dentinogenesis imperfecta shields type II with a novel DSPP mutation.

BACKGROUND: Dentinogenesis imperfecta (DGI), Shields type-II is an autosomal dominant genetic disease which severely affects the function of the patients' teeth. The dentin sialophosphoprotein (DSPP) gene is considered to be the pathogenic gene of DGI-II. In this study, a DGI-II family with a novel DSPP mutation were collected, functional characteristics of DGI cells and clinical features were analyzed to better understand the genotype-phenotype relationship of this disease. METHODS: Clinical data were collected, whole exome sequencing (WES) was conducted, and Sanger sequencing was used to verify the mutation sites. Physical characteristics of the patient's teeth were examined using scanning electron microscopy (SEM) and energy dispersive spectroscopy (EDS). The localization of green fluorescent protein (GFP)-fused wild-type (WT) dentin sialoprotein (DSP) and its variant were evaluated via an immunocytochemistry (ICC) assay. The behaviors of human dental pulp stem cells (hDPSCs) were investigated by flow cytometry, osteogenic differentiation, and quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: A novel heterozygous mutation c.53T > G (p. Val18Gly) in DSPP was found in this family. The SEM results showed that the participants' teeth had reduced and irregular dentinal tubes. The EDS results showed that the Ca/P ratio of the patients' teeth was significantly higher than that of the control group. The ICC assay showed that the mutant DSP was entrapped in the endoplasmic reticulum (ER), while the WT DSP located mainly in the Golgi apparatus. In comparison with normal cells, the patient's cells exhibited significantly decreased mineralization ability and lower expression levels of DSPP and RUNX2. CONCLUSIONS: The c.53T > G (p. Val18Gly) DSPP variant was shown to present with rare hypoplastic enamel defects. Functional analysis revealed that this novel variant disturbs dentinal characteristics and pulp cell behavior.

Elevated levels of soluble Endothelial protein C receptor in rheumatoid arthritis and block the therapeutic effect of protein C in collagen-induced arthritis.

BACKGROUND: Endothelial protein C receptor (EPCR) is a membranous protein that can be combined with a variety of ligands and plays important roles in anticoagulant and anti-inflammation. Recent reports have shown that surface EPCR expression on T cells is negatively associated with Th17 differentiation and is co-expressed with other immunosuppressive molecules, such as The programmed cell death 1 (PD-1) and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4). Hence, we hypothesized that EPCR may play a critical role in rheumatoid arthritis (RA) disease progression that is mediated by Th17 differentiation. In order to explore the role of EPCR on RA disease pathogenesis, we detected membranous EPCR (mEPCR) expression in CD4+ T cells and soluble EPCR (sEPCR) expression in the sera of RA patients. METHODS: The proportion of CD4+/EPCR+ T cells in the peripheral blood of RA patients was detected by flow cytometry, and the expression of sEPCR in the sera of RA patients was detected by enzyme-linked immunosorbent assay (ELISA). For in vitro experiments, protein C (PC) and EPCR recombinant proteins were used to block peripheral blood mononuclear cell (PBMC) activation and to detect Th17 differentiation. For in vivo experiments in DBA/1 mice with collagen-induced arthritis (CIA), we administered PC and EPCR recombinant proteins, monitored disease progression, and evaluated the role of EPCR in disease progression. RESULTS: The proportion of CD4+/EPCR+ T cells in the peripheral blood of RA patients was lower than that of osteoarthritis (OA) patients, while the expression level of sEPCR in the sera of RA patients was concomitantly higher than that in OA patients. Subsequent analysis revealed that sEPCR expression was positively correlated with rheumatoid factors (RF) and other inflammatory indicators in RA patients. Further studies confirmed that sEPCR administration alleviated the progression of collagen-induced arthritis and partially blocked the therapeutic effect of PC in CIA mice. CONCLUSION: Soluble EPCR is associated with RA disease progression and induces disease remission in CIA mice by inhibiting Th17 differentiation.

MicroRNA-140-5p inhibits the tumorigenesis of oral squamous cell carcinoma by targeting p21-activated kinase 4.

Oral squamous cell carcinoma (OSCC) is a serious global health problem. Recently, accumulating microRNA (miRNA) has emerged as crucial players in the development and progression of carcinomas including OSCC. Our study aimed to further investigate the roles of miR-140-5p in OSCC tumorigenesis and related molecular basis. In this study, OSCC tissues and adjacent normal tissues were isolated from 34 OSCC patients who suffered from surgical resection at our hospital. MiR-140-5p level was measured by reverse-transcription quantitative polymerase chain reaction assay. p21-activated kinase 4 (PAK4) protein level was determined by western blot assay in OSCC cells at 48 h posttransfection or OSCC xenograft tumors at day 35 after OSCC cell injection. The cell proliferative ability was assessed by cell counting kit-8 assay in OSCC cells at 0, 24, 48, 72 h after transfection. Cell apoptosis and cell-cycle analysis was conducted using a flow cytometry in OSCC cells at 48 h after transfection. The interaction between miR-140-5p and PAK4 3'-untranslated region was tested by bioinformatics analysis and luciferase reporter assay in OSCC cells at 48 h after transfection. Mouse xenograft models of OSCC were established to examine the influence of miR-140-5p on OSCC tumorigenesis in vivo during 35 days after OSCC cell injection. Our data showed that miR-140-5p expression was notably downregulated in OSCC tissues and cell lines. MiR-140-5p inhibited the expression of PAK4 by direct interaction in OSCC cells. Functional analysis disclosed that miR-140-5p overexpression or PAK4 knockdown suppressed cell proliferation, promoted cell apoptosis, and induced cell-cycle arrest in OSCC. Moreover, PAK4 upregulation rescued the detrimental effects of miR-140-5p on cell proliferation and cell-cycle progression and hampered cell apoptosis induced by miR-140-5p in OSCC. In vivo experiments demonstrated that miR-140-5p overexpression suppressed the growth of OSCC xenograft tumors by downregulating PAK4. In conclusion, our data revealed miR-140-5p suppressed OSCC tumorigenesis by targeting PAK4 in vitro and in vivo, deepening our understanding on the function and molecular basis of miR-140-5p in the development of OSCC.

Polymorphism of a chiral iron(ii) complex: spin-crossover and ferroelectric properties.

Two solvent-free polymorphs of a chiral iron(ii) complex have been obtained, and their polymorphism dependent spin-crossover and ferroelectric properties have been demonstrated. Polymorph I shows a gradual spin-crossover behavior, whereas polymorph II remains in a high-spin state but shows a typical ferroelectric feature.

Spin crossover properties of enantiomers, co-enantiomers, racemates, and co-racemates.

Through multi-component self-assembly of chiral phenylethylamine, 1-alkyl-2-imidazolecarboxaldehyde and iron(ii) ions, two couples of enantiomeric iron(ii) complexes , , and with the formula of fac-Λ or Δ-[Fe(L)3](2+)(L = R or S-1-phenyl-N-(1-alkyl-1H-imidazol-2-ylmethylene)ethanamine) have been designed and synthesized as building blocks. Further binary cocrystallization of the prefabricated enantiomers enabled us to construct spin crossover co-enantiomers and , racemates and , and co-racemate . Compared with in a high spin state and with spin crossover at 291 K, the co-enantiomers exhibited gradual spin crossover at a higher temperature of 301 K, and the racemic alloys showed hysteresis loops induced by desolvation above room temperature. It was demonstrated that molecular chirality could be used effectively for stereochemical engineering of spin crossover materials. In addition, crystal packing, intramolecular π-π stacking, intermolecular C-Hπ interactions and solvent effects were elucidated to be responsible for the distinct spin crossover properties. This collective structural and magnetic study not only enriched the spin crossover library, but also provided a full comparison of optically pure, homochiral, and racemic materials with similar molecular structures.

[Adipose-derived stem cells promote the polarization from M1 macrophages to M2 macrophages].

OBJECTIVE: To investigate the effects of adipose-derived stem cells (ADSCs) on M1/M2 macrophages and whether ADSCs are able to promote the polarization from M1 macrophages to M2 macrophages. METHODS: M1 macrophages were induced from J774.1 macrophages by 24-hour stimulation of lipopolysaccharide (LPS) and interferon γ (IFN-γ), and M2 macrophages were induced from J774.1 macrophages by interleukin 4 (IL-4) for another 24 hours. Then M1/M2 macrophages were separately cultured in the presence of ADSCs for 24 hours. The M1/M2 macrophages and their corresponding supernatants were collected for further analysis. The expressions of IL-6, tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS), CC chemokine ligand 2 (CCL2), CD86, arginase 1 (Arg1), mannose receptors/CD206 (MR/CD206), IL-10, found in inflammatory zone 1 (FIZZ1), chitinase 3-like 3 (Ym-1) were detected by real-time PCR and ELISA. RESULTS: ADSCs significantly decreased the levels of IL-6, TNF-α, iNOS, CCL2 and CD86, and increased the levels of Arg1, CD206 and IL-10 in M1 macrophages. In the supernatant of M1 macrophages, the expressions of IL-6 and TNF-α were reduced, while those of CD206 were enhanced. In M2 macrophages, ADSCs resulted in down-regulation of IL-6, TNF-α, iNOS, CD86 and up-regulation of Arg1, CD206, FIZZ-1, Ym-1 and IL-10. In the supernatant of M2 macrophages, the expression levels of IL-6 and TNF-α were down-regulated and those of CD206 were up-regulated. CONCLUSION: ADSCs can inhibit the gene expression of M1 macrophages and promote the gene expression of M2 macrophages, as well as mediate the polarization from M1 macrophages to M2 macrophages.

Chiral tetrahedral iron(II) cages: diastereoselective subcomponent self-assembly, structure interconversion and spin-crossover properties.

A new class of chiral tetrahedral iron(II) cages were prepared from subcomponent self-assembly with high diastereoselectivity. The cages can be interconverted through imine exchange. The chiral cages displayed a spin transition close to room temperature, and the transition temperatures were affected by the substituent and uncoordinated solvents.

Enantioselective DNA condensation induced by heptameric lanthanum helical supramolecular enantiomers.

DNA condensation induced by a pair of heptameric La(III) helical enantiomers M-[La7(S-L)6(CO3)(NO3)6(OCH3)(CH3OH)7]·2CH3OH·5H2O and P-[La7(R-L)6(CO3)(NO3)6(OCH3)(CH3OH)5(H2O)2]·2CH3OH·4H2O (M-La and P-La, L=2-(2-hydroxybenzylamino)-3-carbamoylpropanoic acid) has been investigated by UV/vis spectroscopy, fluorescence spectroscopy, CD spectroscopy, EMSA, RALS, DLS, and SEM. The enantiomers M-La and P-La could induce CT-DNA condensation at a low concentration as observed in UV/vis spectroscopy. DNA condensates possessed globular nanoparticles with nearly homogeneous sizes in solid state determined by SEM (ca. 250 nm for M-La and ca. 200 nm for P-La). The enantiomers bound to DNA through electrostatic attraction and hydrogen bond interactions in a major groove, and rapidly condensed free DNA into its compact state. DNA decompaction has been acquired by using EDTA as disassembly agent, and analyzed by UV/vis spectroscopy, CD spectroscopy and EMSA. Moreover, the enantiomers M-La and P-La displayed discernible discrimination in DNA interaction and DNA condensation, as well as DNA decondensation. Our study suggested that lanthanum(III) enantiomers M-La and P-La were efficient DNA packaging agents with potential applications in gene delivery.

Dinuclear nickel(II) triple-stranded supramolecular cylinders: syntheses, characterization and G-quadruplexes binding properties.

Three dinuclear nickel triple-stranded supramolecular cylinders [Ni2(L1)3][ClO4]4 (1), [Ni2(L2)3][ClO4]4 (2) and [Ni2(L3)3][ClO4]4 (3) with bis(pyridylimine) Schiff base containing triphenyl groups in the spacers as ligands were synthesized and characterized. The human telomeric G-quadruplexes binding properties of cylinders 1-3 were evaluated by means of UV-Vis spectroscopy, circular dichroism (CD) spectroscopy and fluorescence resonance energy transfer (FRET) melting assay. UV-Vis studies revealed that the supramolecular cylinders 1-3 could bind to G-quadruplex DNA with high binding constants (Kb values ranging from 0.11-2.2×10(6) M(-1)). FRET melting studies indicated that the cylinders 1-3 had much stronger stabilizing effect on G-quadruplex DNA (ΔTm up to 24.5°C) than the traditional cylinder Ni2L3(4+) just containing diphenylmethane spacers (ΔTm=10.6 °C). Meanwhile, cylinders 1-3 were found to have a modest degree of selectivity for the quadruplex DNA versus duplex DNA in competition FRET assays. Moreover, CD spectroscopy revealed that complex 1 could induce G-quadruplex formation in the absence of metal ions solution and convert antiparallel G-quadruplex into hybrid structure in Na(+) solution. These results provided a new insight into the development of supramolecular cylinders as potential anticancer drugs targeting G-quadruplex DNA.

Effects of muscarinic acetylcholine 3 receptor(208-227) peptide immunization on autoimmune response in nonobese diabetic mice.

The second extracellular loop (LFWQYFVGKRTVPPGECFIQFLSEPTITFGTAI, aa 205-237) of muscarinic acetylcholine 3 receptor (M3R) has been reported to be an epitope for autoantibodies generated during certain autoimmune disorders, including Sjögren's syndrome (SS). Autoantibodies against M3R(228-237) have been shown to interfere with the function of M3R. However, few studies have been performed on the M3R(205-227) peptide of the second extracellular loop. In the current study, we sought to investigate the effect of M3R(208-227) peptide immunization on autoimmune response in NOD/LtJ mice. We synthesized the M3R(208-227) peptide and immunized NOD/LtJ mice to investigate whether peptide-specific antibodies could be generated and whether immunization would lead to changes in autoimmune response in NOD/LtJ mice. Our results demonstrate that the secretions of Th-1, Th-2, and Th-17 cytokines are downregulated and lymphocytic infiltration is improved in the salivary glands and lacrimal glands following immunization with M3R(208-227) peptide in NOD/LtJ mice, suggesting that peptide immunotherapy using the M3R(208-227) peptide may represent a potential therapeutic alternative.

[Immunization with 2nd extracellular loop peptide of muscarinic acetylcholine 3 receptor induces the secretion of IL-17 and IFN-γ in NOD-scid mice].

AIM: To evaluate whether or not the changes in the secretions of IL-17 and IFN-γ can be induced by the immunization with 2nd extracellular loop peptide of muscarinic acetylcholine 3 receptor (M3R) in NOD-scid (nonobese diabetic-severe combined immunodeficiency) mice. METHODS: We synthesized the 2nd extracellular loop peptide of M3R and immunized NOD-scid mice subcutaneously with the 1:1 mixture of the peptide and the incomplete Freund's adjuvant (IFA). At day 1, 7, 14, 21 after immunization, tail blood samples were taken to determine the antibody titer and evaluate the secretions of IL-17 and IFN-γ in sera. Meanwhile, we recorded the fluid intake amount per mouse every week. At day 21, all of the NOD-scid mice were killed to measure the concentrations of IL-17 and IFN-γ in cell supernatants. Immunofluorescence staining of lacrimal glands was performed to observe the changes in the secretions of IL-17 and IFN-γ. RESULTS: Compared with the control group, the sera titers of anti-2nd extracellular loop peptide antibodies were significantly higher in 2nd extracellular loop peptide immunized NOD-scid mice at day 14 (P<0.05). The concentrations of IL-17 and IFN-γ increased significantly in sera of the 2nd extracellular loop peptide immunized NOD-scid mice at day 7 and 14 (P<0.01). The concentration of IL-17 maintained at a certain level in the supernatants of spleen cells co-cultured with 2nd extracellular loop peptide, while it decreased significantly in the control groups (P<0.01). Immunofluorescence staining demonstrated that the production of IL-17 and IFN-γ increased in the lacrimal glands of NOD-scid mice immunized with the 2nd extracellular loop peptide. However, no changes in fluid intake was observed in NOD-scid mice immunized with the 2nd extracellular loop peptide(P>0.05). CONCLUSION: Immunization with 2nd extracellular loop peptide of M3R can induce the production of anti-2nd extracellular loop peptide antibodies and the secretions of IL-17 and IFN-γ in NOD-scid mice.

Hexa-kis-(µ2-4-amino-3,5-dimethyl-4H-1,2,4-triazole)hexa-aqua-tricobalt(II) naphthalene-1,5-disulfonate tetra-chloride.

In the centrosymmetric trinuclear cation of the title compound, [Co3(C4H(8)N4)6(H2O)6](C10H6O6S2)Cl4, the three Co(II) atoms are bridged by six triazole mol-ecules via the N atoms in the 1,2-positions. The central Co(II) atom, lying on an inversion center, is coordinated by six triazole N atoms while the terminal Co(II) atoms are coordinated by three triazole N atoms and three water O atoms in a distorted octa-hedral geometry. The naphthalene-disulfonate anion is also centrosymmetric. The four chloride counter anions are half-occupied; the H atoms of the amino groups show an occupancy of 2/3. O-H⋯Cl, O-H⋯O and N-H⋯O hydrogen bonds link the complex cations and the chloride and naphthalene-1,5-disulfonate anions.

[Role of glucocorticoid receptor in the pathogenesis of systemic lupus erythematosus].

OBJECTIVE: To investigate the expressions of GRα mRNA and GRß mRNA in the peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients, in order to reveal the role of GR mRNA in the pathogenesis of SLE and analyze the relationship between GR mRNA and SLEDAI score, dsDNA, cardiovascular involvement. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) technique was applied to semiquantitatively analyze GRα mRNA and GRß mRNA expressions in 104 SLE patients and 56 volunteers. RESULTS: The level of GRα mRNA was lower in the SLE group (the relative level was 1.24±0.97)than in the control group (the relative level was 2.31±1.42, P<0.05), and the level of GRß mRNA was higher in the SLE group(the relative level was 0.61±1.23) than in the control group(the relative level was 0.18±0.21, P<0.05). The level of GRα was lower in the active group (the relative level was 0.68±0.40) than in the inactive group(the relative level was 1.65±1.06, P<0.01), but the level of GRß was higher in the active group(the relative level was 0.88±1.56) than in the inactive group(the relative level was 0.24±0.23, P<0.01); GRα mRNA was related negatively to the SLEDAI score and dsDNA, but GRß mRNA was related positively to the SLEDAI score and dsDNA(P<0.01).The level of GRα mRNA was lower in the dsDNA positive group(the relative level was 0.89±0.66) than in the dsDNA negative group (the level was 1.54±1.10), the level of GRß mRNA was higher in the dsDNA positive group (the relative level was 0.95±1.60) than in the dsDNA negative group (the relative level was 0.22±0.21). The level of GRß mRNA and the value of GRß mRNA/ GRα mRNA was obviously higher in the SLE group with cardiac involvement (the relative level was 1.02 ±1.76, the valve of GRß / GRα was 1.10±2.02)than in the SLE group without cardiac involvement (the relative level was 0.28±0.31, the valve of GRß / GRα was 0.32±0.32, P<0.05), and the level of GRα mRNA wasn't significant in the two groups (P>0.05). CONCLUSION: The levels of GRα mRNA and GRß mRNA maybe play an important role in the pathogenesis of SLE. And the levels of GRα mRNA and GRß mRNA are related to the activity of SLE. The level of GRß mRNA and the value of GRß mRNA/ GRα mRNA are related with cardiovascular involvement in SLE.

A new type of entangled coordination network: coexistence of polythreading and polyknotting involved molecular braids.

A fascinating polythreaded coordination network formed by 1D crankshaft shaped chains threading into a 2D undulated sheet in a one-over/one-under interweaving fashion was reported, in which the 2D layer exhibits an unusual polyknotted entanglement containing triple-stranded molecular braids.