Poly[[bis(μ2-4-amino­benzene­sul­fon­ato-κ2 N:O)diaqua­manganese(II)] dihydrate]

The title compound, {[Mn(NH2C6H4SO3)2(H2O)2]·2H2O}n, was prepared under mild hydro­thermal conditions. The unique MnII ion is located on a crystallographic inversion center and is coordinated by two –NH2 and two –SO3 groups from four 4-amino­benzene­sulfonate ligands and by two water mol­ecules in the axial positions, forming a slightly distorted octa­hedral coordination environment. The 4-amino­benzene­sulfonate anions behave as μ2-bridging ligands to produce a two-dimensional structure. In the crystal structure, inter­molecular N—H⋯O, O—H⋯O and C—H⋯O hydrogen bonds link the layers into a three-dimensional network

Diaqua­bis(2-carboxy­benzoato-κO)nickel(II)

In the title compound, [Ni(C8H5O4)2(H2O)2], the NiII atom lies on an inversion centre and exhibits a square-planar geometry incorporating two phthalate and two water O atoms. The nickel complex is stabilized by intra­molecular inter­actions involving water O atoms and H atoms of the phthalate groups. It forms one-dimensional zigzag chains along the b axis which are held together via π–π stacking inter­actions (3.647 Å) between the benzene rings of the phthalate groups. The adjacent chains are also hydrogen bonded, resulting in a three-dimensional supra­molecular network

α-Lactosylceramide Protects Against iNKT-Mediated Murine Airway Hyperreactivity and Liver Injury Through Competitive Inhibition of Cd1d Binding.

Invariant natural killer T (iNKT) cells, which are activated by T cell receptor (TCR)-dependent recognition of lipid-based antigens presented by the CD1d molecule, have been shown to participate in the pathogenesis of many diseases, including asthma and liver injury. Previous studies have shown the inhibition of iNKT cell activation using lipid antagonists can attenuate iNKT cell-induced disease pathogenesis. Hence, the development of iNKT cell-targeted glycolipids can facilitate the discovery of new therapeutics. In this study, we synthesized and evaluated α-lactosylceramide (α-LacCer), an α-galactosylceramide (α-GalCer) analog with lactose substitution for the galactose head and a shortened acyl chain in the ceramide tail, toward iNKT cell activation. We demonstrated that α-LacCer was a weak inducer for both mouse and human iNKT cell activation and cytokine production, and the iNKT induction by α-LacCer was CD1d-dependent. However, when co-administered with α-GalCer, α-LacCer inhibited α-GalCer-induced IL-4 and IFN-γ production from iNKT cells. Consequently, α-LacCer also ameliorated both α-GalCer and GSL-1-induced airway hyperreactivity and α-GalCer-induced neutrophilia when co-administered in vivo. Furthermore, we were able to inhibit the increases of ConA-induced AST, ALT and IFN-γ serum levels through α-LacCer pre-treatment, suggesting α-LacCer could protect against ConA-induced liver injury. Mechanistically, we discerned that α-LacCer suppressed α-GalCer-stimulated cytokine production through competing for CD1d binding. Since iNKT cells play a critical role in the development of AHR and liver injury, the inhibition of iNKT cell activation by α-LacCer present a possible new approach in treating iNKT cell-mediated diseases

Analysis of Inverse Kinematics and Dynamics of a Novel 6-Degree-of-freedom Wire-Driven Parallel Gantry Crane Robot

Every type of wire-driven parallel robots can be used in cargo handling as a robot crane. Concerning the 6-degree-of-freedom (DOF) wire-driven parallel robot with three wires, its mechanism configuration belongs to URPMs (Under Restrained Positioning Mechanisms), if one translational or rotational DOF rigid mechanism is added to each of its kinematic chains. In this case the mechanism becomes a new type 6-DOF robot. It has been found, in the research survey that the mechanism configuration of such kind of 6-DOF robot CABLEV is not powerful enough because of its limited workspace. A novel 6-DOF parallel crane robot containing three rigid-and-flexible hybrid sub-chains is proposed which can access to a larger workspace. The differential flatness of its inverse kinematics and dynamics is analyzed by a simulation. The results of this simulation will lay a basis for the future trajectory tracking control of the payload

Pulmonary IL- 33 orchestrates innate immune cells to mediate respiratory syncytial virus- evoked airway hyperreactivity and eosinophilia

BackgroundRespiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL- 33 is elevated and promotes immune cell activation, leading to the development of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL- 33- activated innate immune cells, including ILC2s and ST2+ myeloid cells, in RSV infection- triggered pathophysiology.MethodsThe role of IL- 33/ILC2 axis in RSV- induced AHR inflammation and eosinophilia were evaluated in the IL- 33- deficient and YetCre- 13 Rosa- DTA mice. Myeloid- specific, IL- 33- deficient or ST2- deficient mice were employed to examine the role of IL- 33 and ST2 signaling in myeloid cells.ResultsWe found that IL- 33- activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2- derived IL- 13 was sufficient for RSV- driven AHR, since reconstitution of wild- type ILC2 rescued RSV- driven AHR in IL- 13- deficient mice. Meanwhile, myeloid cell- derived IL- 33 was required for airway inflammation, ST2+ myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL- 33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL- 33 signaling.ConclusionsThis study highlights the importance of IL- 33- activated ILC2s in mediating RSV- triggered AHR and eosinophilia. In addition, IL- 33 signaling in myeloid cells is crucial for airway inflammation.Respiratory syncytial virus induces ILC2 to produce IL- 5 and IL- 13 through IL- 33, which is crucial for the development of airway hyperreactivity and airway inflammation. Myeloid cell- derived IL- 33 and suppression of tumorigenicity 2- positive myeloid cells contribute to cytokine production and cellular inflammation in airway. Both ILC2 and myeloid cell IL- 33 signaling contribute to local and peripheral eosinophilia.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/1/all14091.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/2/all14091-sup-0001-Supinfo.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/3/all14091_am.pd

Nuclear Receptor Interaction Protein (NRIP) expression assay using human tissue microarray and immunohistochemistry technology confirming nuclear localization

Background: A novel human nuclear receptor interaction protein (NRIP) has recently been discovered by Chen SL et al , which may play a role in enhancing the transcriptional activity of steroid nuclear receptors in prostate (LNCaP) and cervical (C33A) cancer cell lines. However, knowledge about the biological functions and clinical implications of NRIP, is still incomplete. Our aim was to determine the distribution of NRIP expression and to delineate the cell types that express NRIP in various malignant tumors and healthy non-pathological tissues. This information will significantly affect the exploration of its physiological roles in healthy and tumor cells. Methods: By using tissue microarray (TMA) technology and an anti-NRIP monoclonal antibody immunohistochemical (IHC) survey, NRIP expression was examined in 48 types of tumors and in a control group of 48 matched or unmatched healthy non-neoplastic tissues. Results: Our survey results showed that ten cases were revealed to express the NRIP in six malignancies (esophageal , colon, breast, ovarian, skin, and pancreatic cancers), but not all of these specific tumor types consistently showed positive NRIP expression. Moreover, malignant tumors of the stomach, prostate, liver, lung, kidney, uterine cervix, urinary bladder, lymph node, testis, and tongue revealed no NRIP expression. Among the control group of 48 matched and unmatched nonneoplastic tissues, all of them demonstrated IHC scores less than the cut-off threshold of 3. In addition , ten cores out of thirty-six carcinomatous tissues revealed positive NRIP expression, which indicated that NRIP expression increases significantly in carcinoma tissue cores , comparing to the matched controlled healthy tissues. Conclusion: This is the first study to use a human TMA and IHC to validate the nuclear localization for this newly identified NRIP expression. In considering the use of NRIP as a potential diagnostic tool for human malignancies survey , it is important to note that NRIP expression carries a sensitivity of only 23%, but has a specificity of 100%. There is also a significant difference in positive NRIP expression between primary carcinomatous tissues and matched controlled healthy tissues. Although further large-scale studies will merit to be conducted to evaluate its role as a potential adjunct for cancer diagnosis, data from this study provides valuable references for the future investigation of the biological functions of NRIP in humans

Galaxy source counts at 7.7 μ\mum, 10 μ\mum and 15 μ\mum with the James Webb Space Telescope

We present mid-infrared galaxy number counts based on the Early Release Observations obtained by the James Webb Space Telescope (JWST) at 7.7-, 10- and 15-$\mu$m (F770W, F1000W and F1500W, respectively) bands of the Mid-Infrared Instrument (MIRI). Due to the superior sensitivity of JWST, the 80 percent completeness limits reach 0.32, 0.79 and 2.0 $\mu$Jy in F770W, F1000W and F1500W filters, respectively, i.e., $\sim$100 times deeper than previous space infrared telescopes such as Spitzer or AKARI. The number counts reach much deeper than the broad bump around $0.05\sim0.5$ mJy due to polycyclic aromatic hydrocarbon (PAH) emissions. An extrapolation towards fainter flux from the evolutionary models in the literature agrees amazingly well with the new data, where the extrapolated faint-end of infrared luminosity functions combined with the cosmic star-formation history to higher redshifts can reproduce the deeper number counts by JWST. Our understanding of the faint infrared sources has been confirmed by the observed data due to the superb sensitivity of JWST.Comment: 6 pages, 8 figures. Accepted for publication in MNRA