Coexistence of Two Different Distorted Octahedral [MnF6 ]3- Sites in K3 [MnF6 ]: Manifestation in Spectroscopy and Magnetism.

As a consequence of the static Jahn-Teller effect of the 5 E ground state of MnIII in cubic structures with octahedral parent geometries, their octahedral coordination spheres become distorted. In the case of six fluorido ligands, [MnF6 ]3- anions with two longer and four shorter Mn-F bonds making elongated octahedra are usually observed. Herein, we report the synthesis of the compound K3 [MnF6 ] through a high-temperature approach and its crystallization by a high-pressure/high-temperature route. The main structural motifs are two quasi-isolated, octahedron-like [MnF6 ]3- anions of quite different nature compared to that met in ideal octahedral MnIII Jahn-Teller systems. Owing to the internal electric field of Ci symmetry dominated by the next-neighbour K+ ions acting on the MnIII sites, both sites, the pseudo-rhombic (site 1) and the pseudo-tetragonally elongated (site 2) [MnF6 ]3- anions are present in K3 [MnF6 ]. The compound was characterized by single-crystal and powder X-ray diffraction, and magnetometry as well as by FTIR, Raman, and ligand field spectroscopy. A theoretical interpretation of the electronic structure and molecular geometry of the two Mn sites in the lattice is given by using a vibronic coupling model with parameters adjusted from multireference ab-initio cluster calculations.

HF-Free Synthesis of Li2SiF6:Mn4+: A Red-Emitting Phosphor.

Li2SiF6:Mn4+ was synthesized via a new HF-free synthesis route by a high-pressure/high-temperature doping experiment at 5.5 GPa and 750 °C. It is proven that the phosphor cannot be synthesized by the common wet-chemical precipitation route in aqueous HF. The sample was characterized by powder X-ray diffraction, EDX, and luminescence spectroscopy. At room temperature, Li2SiF6:Mn4+ exhibits seven emission lines with the strongest line at λmax ≈ 630 nm and a dominant wavelength of λdom ≈ 618 nm. The CIE coordinates are 0.688 and 0.312 for x and y, respectively. The compound shows a luminous efficacy of radiation (LER) of 218 lm Wopt-1, which exceeds the LER of current state-of-the-art red LED phosphor K2SiF6:Mn4+ by 7% due to a blue-shift of the emission. It reveals excellent thermal quenching behavior up to 125 °C.

Short-Range Antiferromagnetic Ordering of Netlike S = 1/2 Linear Trimeric Units in the Copper Germanate K2Cu3Ge4O12.

K2Cu3Ge4O12 was synthesized via a solid-state reaction in a high-temperature experiment at 1073 K. Crystal structure analysis provided the following data: space group Cmcm (no. 63), a = 1407.9(2), b = 578.0(1), c = 1389.2(1) pm, V = 1.1305 nm3, and Z = 4. The structure consists of alternating layers of netlike arranged trimeric [Cu3O8]10- units and layers of four-membered rings of GeO4 tetrahedra. The potassium cations connect the different structural moieties. Although both structural motifs are well-known, the way they are connected in K2Cu3Ge4O12 is unique. K2Cu3Ge4O12 was further characterized via vibrational spectroscopy and SEM-EDX measurements. Magnetic measurements exhibit an antiferromagnetic behavior at low temperatures along with an unusual pseudo-2D coupling.

Europium Lithosilicates Li2EuSi2N4 and Li2EuSiO4-Crystal Structures and Luminescence.

With Li2EuSi2N4, the end member of the solid-solution series set up by substituting the divalent cation in the well-known host materials Li2CaSi2N4 and Li2SrSi2N4 with Eu(II) could be synthesized and described by means of single-crystal X-ray diffraction and single-grain luminescence spectroscopy. The new compound crystallizes isotypically to Li2CaSi2N4 and Li2SrSi2N4 in cubic space group Pa3̅ (no. 205) with a lattice parameter of a = 10.7049(2) Å and a cell volume of V = 1226.73(7) Å3. Irradiated with blue light, Li2EuSi2N4 exhibits a narrow-band red emission (λmax = 628 nm, 1.97 eV, 15924 cm-1; fwhm = 83 nm, 0.27 eV, 2143 cm-1). Also for Li2EuSiO4, the end member of the solid-solution series of Li2SrSiO4 with Sr(II) substituted by Eu(II), luminescence emission could be measured on a single crystal (λmax = 595 nm, 2.05 eV, 16798 cm-1; fwhm = 116 nm, 0.40 eV, 3211 cm-1). In this paper, both compounds are being compared with other known members of their solid-solution series regarding structure and luminescence properties.

Isomorphism of Sr[Li3AlO4] and Sr[Li3GaO4] - Syntheses, Crystal Structure, and Europium(II) Luminescence.

While highly efficient red-emitting inorganic phosphors have been discovered in the substance class of alkaline earth oxo(nitrido)lithoaluminates, new narrow-band green- and yellow-emitting components are being sought to improve the performance of phosphor-converted light-emitting diodes (pc-LEDs). Various solid-state reactions were carried out under protective gas atmosphere in nickel crucibles and sealed tantalum ampules to synthesize Sr[Li3AlO4], Sr[Li3GaO4], and five substitutional derivates of Sr[Li3(Al1-x Ga x )O4] at moderate temperatures. The observation of a linear increase in the unit cell parameters as a function of the increasing gallium mole fraction x in Sr[Li3(Al1-x Ga x )O4] revealed Vegard behavior in the solid-solution series, which was derived from powder X-ray diffraction data. The isomorphic crystallization of the new oxolithogallate Sr[Li3GaO4] and the known oxolithoaluminate Sr[Li3AlO4] in an ordered variant of the U[Cr4C4] aristotype was verified on the basis of powder and single-crystal X-ray diffraction data. Photoluminescence spectroscopy was used to investigate the narrow-band emissions in the substitution series of Eu2+-activated Sr[Li3(Al1-x Ga x )O4] under blue-light excitation. The emission maximum was shifted to higher energies as the gallium mole fraction increased. Peak wavelengths were observed at λem = 572 nm (fwhm equals 47 nm, 1446 cm-1, 0.18 eV) for yellow-emitting Sr[Li3AlO4]:Eu2+ and at λem = 554 nm (fwhm equals 49 nm, 1589 cm-1, 0.20 eV) for green-emitting Sr[Li3GaO4]:Eu2+. Sr[Li3AlO4]:Eu2+ has excellent thermal quenching resistance with a photoluminescence emission intensity of >93% at T = 423 K relative to the room temperature value, making this inorganic phosphor a potential candidate for solid-state lighting applications.

Human hamstring tenocytes survive when seeded into a decellularized porcine Achilles tendon extracellular matrix.

Tendon ruptures and defects remain major orthopaedic challenges. Tendon healing is a time-consuming process, which results in scar tissue with an altered biomechanical competence. Using a xenogeneic tendon extracellular matrix (ECM) as a natural scaffold, which can be reseeded with autologous human tenocytes, might be a promising approach to reconstruct damaged tendons. For this purpose, the porcine Achilles (AS) tendons serving as a scaffold were histologically characterized in comparison to human cell donor tendons. AS tendons were decellularized and then reseeded with primary human hamstring tenocytes using cell centrifuging, rotating culture and cell injection techniques. Vitality testing, histology and glycosaminoglycan/DNA quantifications were performed to document the success of tendon reseeding. Porcine AS tendons were characterized by a higher cell and sulfated glycosaminoglycan content than human cell donor tendons. Complete decellularization could be achieved, but led to a wash out of sulfated glycosaminoglycans. Nevertheless, porcine tendon could be recellularized with vital human tenocytes. The recellularization led to a slight increase in cell number compared to the native tendon and some glycosaminoglycan recovery. This study indicates that porcine tendon can be de- and recellularized using adult human tenocytes. Future work should optimize cell distribution within the recellularized tendon ECM and consider tendon- and donor species-dependent differences.

Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice.

BACKGROUND: Complement represents a crucial mediator of neuroinflammation and neurodegeneration after traumatic brain injury. The role of the terminal complement activation pathway, leading to generation of the membrane attack complex (MAC), has not been thoroughly investigated. CD59 is the major regulator of MAC formation and represents an essential protector from homologous cell injury after complement activation in the injured brain. METHODS: Mice deleted in the Cd59a gene (CD59a-/-) and wild-type littermates (n = 60) were subjected to focal closed head injury. Sham-operated (n = 60) and normal untreated mice (n = 14) served as negative controls. The posttraumatic neurological impairment was assessed for up to one week after trauma, using a standardized Neurological Severity Score (NSS). The extent of neuronal cell death was determined by serum levels of neuron-specific enolase (NSE) and by staining of brain tissue sections in TUNEL technique. The expression profiles of pro-apoptotic (Fas, FasL, Bax) and anti-apoptotic (Bcl-2) mediators were determined at the gene and protein level by real-time RT-PCR and Western blot, respectively. RESULTS: Clinically, the brain-injured CD59a-/- mice showed a significantly impaired neurological outcome within 7 days, as determined by a higher NSS, compared to wild-type controls. The NSE serum levels, an indirect marker of neuronal cell death, were significantly elevated in CD59a-/- mice at 4 h and 24 h after trauma, compared to wild-type littermates. At the tissue level, increased neuronal cell death and brain tissue destruction was detected by TUNEL histochemistry in CD59a-/- mice within 24 hours to 7 days after head trauma. The analysis of brain homogenates for potential mediators and regulators of cell death other than the complement MAC (Fas, FasL, Bax, Bcl-2) revealed no difference in gene expression and protein levels between CD59a-/- and wild-type mice. CONCLUSION: These data emphasize an important role of CD59 in mediating protection from secondary neuronal cell death and further underscore the key role of the terminal complement pathway in the pathophysiology of traumatic brain injury. The exact mechanisms of complement MAC-induced secondary neuronal cell death after head injury require further investigation.

Cold fluorescent light as major inducer of lipid oxidation in soybean oil stored at household conditions for eight weeks.

Light, temperature, and oxygen availability has been shown to promote rancidity in vegetable oils. However, the contribution of each of these environmental factors to lipid oxidation in oil stored under household conditions is not known. We aimed to identify the major inducer of oxidative deterioration of soybean oil stored at constant (67.0 mL) or increasing (67.0-283 mL) headspace volume, 22 or 32 °C, with or without illumination by cold fluorescent light for 56 days by means of fatty acid composition, peroxide value, formation of conjugated dienes, lipid radicals, hexanal, and the decrease in the contents of tocopherols. Soybean oil stored in the dark for 56 days showed an increase of the peroxide value by 124 ± 0.62% (p = 0.006), whereas exposure of the oil to light in a cycle of 12 h light alternating with 12 h darkness for 56 days led to a rise of the peroxide value by 1473 ± 1.79% (p ≤ 0.001). Little effects on the oxidative status of the oil were observed after elevating the temperature from 22 to 32 °C and the headspace volume from 67.0 to 283 mL during 56 days of storage. We conclude that storing soybean oil in transparent bottles under household conditions might pose an increased risk for accelerated lipid oxidation induced by exposure to cold fluorescent light.

Complement gene expression is regulated by pro-inflammatory cytokines and the anaphylatoxin C3a in human tenocytes.

Interplay between complement factors, regulatory proteins, anaphylatoxins and cytokines could be involved in tendon healing and scar formation. The expression and regulation of complement factors by cytokines or anaphylatoxins are completely unclear in tendon. Hence, the gene expression of the anaphylatoxin receptors C3aR, C5aR and cytoprotective complement regulatory proteins (CRPs) was analysed in human tendon, cultured primary tenocytes and to directly compare the general expression level, additionally in human leukocytes. Time-dependent regulation of complement by cytokines and the anaphylatoxin C3a was assessed in cultured tenocytes. Gene expression of the anaphylatoxin receptors C3aR, C5aR and the CRPs CD46, CD55 and CD59 was detected in tendon, cultured tenocytes and leukocytes, whereas CD35 could only be found in tendon and leukocytes. Compared with cultured tenocytes, complement expression was higher in tendon and compared with leukocytes C3aR, C5aR, CD35 and CD55, but not CD46 and CD59 gene expression levels were lower in tendon. C3aR mRNA was up-regulated by both TNFα and C3a in cultured tenocytes in a time-dependent manner whereby C5aR gene expression was only induced by C3a. IL-6 or C3a impaired the CRP gene expression. C3a stimulation lead to an up-regulation of TNFα and IL-1ß mRNA in tenocytes. Degenerated tendons revealed an increased C5aR and a reduced CD55 expression. The expression profile of the investigated complement components in tendon and cultured tenocytes clearly differed from that of leukocytes. Tenocytes respond to the complement split fragment C3a with CRP suppression and enhanced pro-inflammatory cytokine gene expression suggesting their sensitivity to complement activation.

Healing parameters in a rabbit partial tendon defect following tenocyte/biomaterial implantation.

Although rabbits are commonly used as tendon repair model, interpretative tools are divergent and comprehensive scoring systems are lacking. Hence, the aim was to develop a multifaceted scoring system to characterize healing in a partial Achilles tendon defect model. A 3 mm diameter defect was created in the midsubstance of the medial M. gastrocnemius tendon, which remained untreated or was filled with a polyglycolic-acid (PGA) scaffold + fibrin and either left cell-free or seeded with Achilles tenocytes. After 6 and 12 weeks, tendon repair was assessed macroscopically and histologically using self-constructed scores. Macroscopical scoring revealed superior results in the tenocyte seeded PGA + fibrin group compared with the controls at both time points. Histology of all operated tendons after 6 weeks proved extracellular matrix (ECM) disorganization, hypercellularity and occurrence of irregular running elastic fibres with no significance between the groups. Some inflammation was associated with PGA implantation and increased sulphated proteoglycan deposition predominantly with the empty defects. After 12 weeks defect areas became hard to recognize and differences between groups, except for the increased sulphated proteoglycans content in the empty defects, were almost nullified. We describe a partial Achilles tendon defect model and versatile scoring tools applicable for characterizing biomaterial-supported tendon healing.

Extracellular matrix expression of human tenocytes in three-dimensional air-liquid and PLGA cultures compared with tendon tissue: implications for tendon tissue engineering.

Tenocyte transplantation may prove to be an approach to support healing of tendon defects. Cell-cell and cell-matrix contacts within three-dimensional (3D) cultures may prevent tenocyte dedifferentiation observed in monolayer (2D) culture. The present study compares both neotissue formation and tenocyte extracellular matrix (ECM) expression in 2D and 3D cultures directly with that of native tendon, in order to determine optimal conditions for tendon tissue engineering. Primary human tenocytes were embedded in poly[lactic-co-glycolic-acid] (PLGA)-scaffolds and high-density cultures. Neotissue formation was examined by hematoxyline-eosine (H&E) and immunofluorescence staining. Gene expression of ECM proteins and vascular endothelial growth factor (VEGF) was compared at days 0 (2D), 14, and 28 in 3D cultures and tendon. Histomorphology of 3D culture showed tendon-like tissue as tenocyte cell nuclei became more elongated and ECM accumulated. Type I collagen gene expression was higher in 2D culture than in tendon and decreased in 4-week-old 3D cultures, whereas type III collagen was only elevated in high-density culture compared with tendon. Decorin and COMP were reduced in 2D and increased in 3D culture almost to ex vivo level. These results suggest that the 3D high-density or biodegradable scaffolds cultures encourage the differentiation of expanded monolayer tenocytes in vitro to tendon-like tissue.

Effect of pro-inflammatory and immunoregulatory cytokines on human tenocytes.

Tendon injury induces a local inflammatory response, characterized by the induction of pro-inflammatory cytokines. The aim of the present study was to analyze the effects of TNFalpha, IL-6 and IL-10 on key parameters of tendon homeostasis. Cultured primary human tenocytes were treated with the recombinant cytokines IL-6, IL-10, TNFalpha, or combinations of TNFalpha with IL-6 and IL-10 (10 ng/mL, 6, 24 h). Expression of type I collagen, elastin, MMP-1, TNFalpha, IL-1beta, IL-6, IL-10, and suppressors of cytokine signaling (SOCS1, 3) was analyzed with the use of RTD-PCR, immunocytochemistry, and Western blot analysis. In response to TNFalpha, tenocytes reduced their type I collagen deposition but increased their elastin gene expression and highly upregulated their expression for MMP-1, pro-inflammatory (TNFalpha, IL-1beta) and immunoregulatory (IL-6, IL-10) cytokines. TNFalpha stimulation augmented SOCS1, whereas SOCS3 expression in tenocytes was also induced by IL-6. The treatment of tenocytes with IL-6 and IL-10 had no effect on cytokine expression. Neither IL-6 nor IL-10 modulated the observed effects of TNFalpha significantly. These results indicate that TNFalpha strongly activates the tenocytes to amplify their own TNFalpha expression and, subsequently, that of other regulatory cytokines and matrix degrading enzymes. However, the impact of IL-6 and IL-10 on tenocytes remains unclear.