Search

Delocalized Bloch electrons and the low-energy correlations between them determine key optical1, electronic2and entanglement3functionalities of solids, all the way through to phase transitions4,5. To directly capture how many-body correlations affect the actual motion of Bloch electrons, subfemtosecond (1 fs = 10−15s) temporal precision6–15is desirable. Yet, probing with attosecond (1 as = 10−18s) high-energy photons has not been energy-selective enough to resolve the relevant millielectronvolt-scale interactions of electrons1–5,16,17near the Fermi energy. Here, we use multi-terahertz light fields to force electron–hole pairs in crystalline semiconductors onto closed trajectories, and clock the delay between separation and recollision with 300 as precision, corresponding to 0.7% of the driving field’s oscillation period. We detect that strong Coulomb correlations emergent in atomically thin WSe2shift the optimal timing of recollisions by up to 1.2 ± 0.3 fs compared to the bulk material. A quantitative analysis with quantum-dynamic many-body computations in a Wigner-function representation yields a direct and intuitive view on how the Coulomb interaction, non-classical aspects, the strength of the driving field and the valley polarization influence the dynamics. The resulting attosecond chronoscopy of delocalized electrons could revolutionize the understanding of unexpected phase transitions and emergent quantum-dynamic phenomena for future electronic, optoelectronic and quantum-information technologies.

The mechanisms responsible for matrix-assisted laser desorption/ionization (MALDI) are far from being well understood, particularly where infrared laser irradiation is used to initiate the process. We measured the emission yields and kinetic energy distributions of positive ions emitted from 2,5-dihydroxybenzoic acid loaded with angiotensin II in a standard MALDI preparation during irradiation with an infrared free-electron laser tuned to 2.94 µm. As the laser intensity is scanned through the MALDI threshold, we see a marked change in the energy distributions of the matrix ion. Above threshold, the energy distributions of both analyte and matrix cations are constant over a broad range of laser intensities. This behavior does not appear to be consistent with any extant model of the MALDI mechanism. Copyright © 2001 John Wiley & Sons, Ltd.

Purpose We compared detection rates of glaucomatous visual field defects (VFDs) between a conventional rectangular stimulus grid and locally condensed test point arrangements in morphologically suspicious regions.Methods Humphrey Field Analyzer model 630 (HFA I, program 30-2 with a rectangular 6° × 6° grid) was used as the conventional perimetric method. Individual local test-point condensation was realized by fundus-oriented perimetry (FOP) on the Tuebingen Computer Campimeter (TCC).Results Of a total of 66 glaucoma patients, or suspected sufferers, 23 showed normal findings and 27 showed pathological findings with both methods. In 15 cases we found normal visual fields in HFA 30-2, whereas FOP revealed early glaucomatous functional damage. Only one case showed pathological HFA results, while FOP was normal. Detection rates of VFDs significantly differed between the two methods (p < 0.001; sign test).Conclusions FOP, using individually condensed test grids, significantly increases detection rates of glaucomatous VFDs in morphologically suspicuous areas compared with a conventional HFA 30-2 technique using equidistant rectangular (6° × 6°) test point arrangements.

Purpose Transforming growth factor-β1 (TGF-β1) is thought to play a pivotal role in the regulation of the wound healing process after glaucoma filtering surgery. The aim of the present study was to investigate whether platelet-derived growth factor isoforms (PDGF-AA, PDGF-BB), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), in-terleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1) modulate the production of latent and/or active TGF-β1 by cultured human Tenon's capsule fibroblasts (HTF).Methods Human Tenon's capsule fibroblasts were seeded at two different densities (30 cells/mm2and 150 cells/mm2) and stimulated for five days with PDGF-AA, PDGF-BB, bFGF, EGF, IL-1β and TGF-β1. Control cells were treated with serum-free medium (WM/F12). The concentrations of latent and active TGF-β1 in the medium were determined using an immunoassay before and after activation of TGF-β1 by transient acidification.Results The concentration of latent TGF-β1 in conditioned media from HTF seeded at high density (150 cells/mm2) significantly increased after stimulation with 5 ng/ml TGF-β1 (151.5 ± 41.7 pg/ml) or 10 ng/ml IL-1β (45.7 ± 8.1 pg/ml). The concentration of active TGF-β1 in conditioned media also significantly increased after stimulation of HTF with 5 ng/ml TGF-β1 (48.4 ± 27.5 pg/ml).Conclusions The present results indicate that TGF-β1 is the most potent inducer of its own synthesis in HTF. Activation of an autocrine TGF-β1 loop may play a role in the wound healing response after glaucoma filtering surgery.

The contrasting behavior of the trialkoxysilyl-substituted iron metalate [Et3NH][Fe{Si(OMe)3}(CO)3(η¹-dppm)] toward [MCl2(η²-dppm)] (M = Pd, Pt) has been investigated. It reacts with [PdCl2(η²-dppm)] to give the known heterodinuclear complex [Fe(CO)3{μ-Si(OMe)2(OMe)}(μ-dppm)PdCl] (2), although this requires displacement of the Pd-bound chelating dppm ligand. In contrast, reaction with [PtCl2(η²-dppm)] afforded [Fe(CO)3(μ-dppm)2Pt{Si(OMe)3}Cl] (3), which results from silyl migration from Fe to Pt. This intermetallic silyl migration reaction has very few precedents and is observed here for the first time in bimetallic dppm complexes. Loss of the silyl ligand of 3 occurs slowly in CH2Cl2 and leads to [FeCl(CO)(μ-CO)(μ-dppm)2PtCl] (4). This A-frame complex is protonated by HBF4 to give [FeCl(CO)2(μ-dppm)2Pt(H)Cl][BF4] (5).

High-intensity electrical stimulation of the trigeminal ganglion is accompanied by mast cell degranulation, vasodilatation, increased endothelial permeability and leakage of albumin from postcapillary venules within the dura mater. Overall, the histological appearance suggests an evolving sterile inflammatory response. This neurogenic inflammation within the meninges has been suggested as a model to explain the pain in migraine and cluster headache, and has been used to characterize the pharmacology of anti-migraine compounds. Using the rat model of neurogenic inflammation, the albumin extravasation ratio (stimulated : unstimulated side) in vehicle-treated animals in the dura and retina was 1.60 ± 0.11 and 1.76 ± 0.18, respectively (n = 10; values are mean ± SEM). Pretreatment with sumatriptan (n = 9) produced a highly significant reduction in the ratio of extravasation within the dura to 1.10 ± 0.06 (P = 0.002) and in the retina to 0.96 ± 0.06 (P ± 0.001), as did the neurokinin-1 receptor antagonist RP 67580 (n = 12) in the dura (1.04 ± 0.11, P = 0.002) and retina (1.08 ± 0.06, P = 0.001). These data demonstrate increased endothelial permeability and leakage of albumin not only in the dura but also in the retina. In a second stage we investigated possible extravasation in the human retina in acute migraine (n = 8) and cluster headache (n = 5) using fluorescein or indocyanine angiography. No increased endothelial permeability or leakage of dye could be found in the human retinal or choroidal vessels during headache attacks or in the headache-free interval in persons suffering from both migraine and cluster headache. These data raise the possibility that neurogenic inflammation is not a major factor in headache attacks in migraine or cluster headache.Keywords:migraine attack; neurogenic inflammation; trigeminovascular system; plasma extravasation; fluorescein angiography

PURPOSE. Several previous studies have shown that glycoconjugates of extracellular matrix, cell membrane and nucleus play an important role in the mediation of cell proliferation, migration and differentiation. Lens epithelial cells and lens fiber cells show regional differences with regard to these parameters. If glycoconjugates participate in the regulation of these patterns in the lens, there should be regional differences in the expression of glycoconjugates. The investigation was focused on the anterior pole, equator and nuclear bow regions, which differ extensively in lens cell proliferation and differentiation. METHODS. To check this hypothesis, the regional binding pattern of twelve different FITC-conjugated lectins was studied glycohistochemically, using paraffin embedded material. The investigation was focused on the anterior pole, equator and nuclear bow regions. RESULTS. Regional differences in lectin binding patterns were identified in the lens capsule, epithelium and the nuclear bow regions. The lens capsule was fluorescently labeled with GS-I, UEA-I, LPA, MAA, SNA only at the anterior pole and with CON-A, WGA, DBA, SBA only at the equator. Staining of the entire anterior surface of the lens capsule was observed with LFA. Cell membranes of the lens epithelium showed binding of MAA and LFA only at the equator. LFA, LPA, MAA and SNA only stained the nuclei of fiber cells at the nuclear bow region but not of lens epithelial cells. WGA strongly labeled the nuclei of equatorial epithelial cells and fiber cells at the bow region. CONCLUSIONS. It is assumed that the observed regional variations in glycoprotein expression in the extracellular matrix and lens cells contribute to the regulation of cell behavior in different areas of the lens.

Addition of RNC to the heterobimetallic acyl complex [(OC)3Fe{μ-Si(OMe)2(OMe)}(μ-dppm)Pt{C(O)Me}] (1a), which displays a μ−η²-Si−O bridge, afforded the isonitrile adducts [(OC)3{(MeO)3Si}Fe(μ-dppm)Pt{C(O)Me}(C&tbd1;NR)] (3a R = t-Bu, 3b R = 2,6-xylyl). Upon treatment of a CH2Cl2 solution of 1a with MeO2CC&tbd1;CCO2Me (DMAD), alkyne insertion into the Pt−C bond gave the alkenyl complex [(OC)3Fe{μ-Si(OMe)2(OMe)}(μ-dppm)Pt{(MeO2C)C&dbd;C(CO2Me)C(O)Me}] 4. The isonitrile adducts [(OC)3{(MeO)3Si}Fe(μ-dppm)Pt{(MeO2C)C&dbd;C(O2Me)C(O)Me}(C&tbd1;NR)] (5a R = t-Bu, 5b R = 2,6-xylyl)] were isolated after addition of RNC. A more complex reaction occurred when phenylacetylene or tert-butylacetylene were reacted with 1a. The iron-bound Si(OMe)3 group and the organic ligand coordinated on platinum were eliminated, and the vinylidene-bridged complexes [(OC)3Fe{μ-C&dbd;C(H)R}(μ-dppm)Pt(CO)] (6a R = Ph, 6b R = t-Bu, 6c R = n-Bu) were obtained. The loosely Pt-bound CO ligand of 6a−c was readily displaced by PPh3, P(OMe)3, or 2,6-xylyl isonitrile yielding the substitution products [(OC)3Fe{μ-C&dbd;C(H)R}(μ-dppm)Pt(L)] (7a R = Ph, L = PPh3; 7b R = t-Bu, L = PPh3; 7c R = t-Bu, L = P(OMe)3; 7d R = t-Bu, L = 2,6-xylylNC). The heterobimetallic phenyl complex [(OC)3Fe{μ-Si(OMe)2(OMe)}(μ-dppm)Pt(Ph)] (8) was obtained by reaction of K[Fe{Si(OMe)3}(CO)3(η¹-dppm)] with a cold THF solution of [PtCl(Ph)(1,5-COD)]. The μ−η²-Si−O bridge is readily opened under a CO atmosphere to give the CO adduct [(OC)3Fe{Si(OMe)3}(μ-dppm)Pt(CO)(Ph)] (9), which unexpectedly does not insert CO into the Pt−phenyl bond. This complex reversibly loses the CO ligand under reduced pressure to regenerate 8. All complexes have been studied by multinuclear NMR spectroscopy. The solid state structures of complexes 3a and 7a have been determined by single-crystal X-ray diffraction.

Low density lipoprotein (LDL), at concentrations high enough for receptor binding but not high enough to saturate the receptor, induces activation of phosphatidylinositol (PtdIns) turnover in a variety of cell types with various biological functions. Using both biochemical and electron microscopic studies, we have shown that blood platelets take up and degrade LDL in a manner reminiscent of phagocytic cell types. The activation of both PtdIns turnover and LDL metabolism is inhibited by high density lipoprotein. Thus, LDL at hormonal concentrations causes general cellular activation. Since all cell types studied responded to LDL with increased PtdIns turnover and uptake of LDL cholesterol, the PtdIns cycle may also be involved in the cellular regulation of LDL cholesterol metabolism.

The heterodinuclear μ-carbonyl complexes [(OC)4M(μ-CO)(μ-dppa)Pt(PPh3)] (3a, M = Mo; 3b, M = W) are formed upon the reaction of [(OC)5M(η¹-dppa)] (1a, M = Mo; 1b, M = W) with [Pt(C2H4)(PPh3)2]. After addition of p-tosylmethyl isonitrile to 3, the CO bridge is replaced by a bridging isonitrile ligand to afford [(OC)4W(μ-C&dbd;NCH2SO2p-tolyl)(μ-dppa)Pt(PPh3)] (4a, M = Mo; 4b, M = W). If stronger electron-donating isonitriles such as benzyl or 2,6-xylyl isonitrile are added to 3, fragmentation into mononuclear complexes occurs. Protonation of 4 leads to the μ-aminocarbyne complexes [(OC)4M{μ-CN(H)CH2SO2p-tolyl}(μ-dppa)Pt(PPh3)][BF4] (5a, M = Mo; 5b, M = W), which react further with isonitriles to yield the μ-aminocarbyne complexes [(OC)3(RNC)W{μ-CN(H)CH2SO2p-tolyl}(μ-dppa)Pt(PPh3)][BF4] 6, (R = 2,6-xylyl, benzyl). Purging a solution of 4a with SO2 yields the complex [(OC)4Mo(μ-SO2)(μ-dppa)Pt(PPh3)], 7a, in which a triphenylphosphine oxide ligand is bound via a hydrogen bridge to the N−H group of the dppa backbone. X-ray diffraction studies performed on 4b and 7a reveal that the μ-CNR and the μ-SO2 ligands bridge the metal centers in an asymmetric manner, the Pt−μ-C or Pt−μ-S distances being significantly shorter than the corresponding W−μ-C or Mo−μ-S distances, respectively.

The success of glaucoma filtration surgery depends mainly on an incomplete wound healing process in the area of the fistula. Since Kornblueth and Tenenbaum's investigations in 1956 it has been known that aqueous humour has intrinsic antiproliferative properties. It is assumed that ascorbic acid is involved in the regulation of the wound healing process after filtration surgery. To evaluate the antiproliferative effect of ascorbic acid in vitro, we used cultured fibroblasts of bovine Tenon's capsule and bovine sclera. Incubation of these cells with ascorbic acid at concentrations ranging from 0.5 to 3 mM/L led to dose-dependent inhibition of cell proliferation. The half-maximal inhibitory concentration was 1.0 mM/L for both cell types. Physiological concentrations of ascorbic acid may be valuable in the pharmacological prevention of failure of glaucoma filtration surgery. However, extensive clinical investigations are needed to clarify whether topical intraoperative or postoperative as well as oral administration of ascorbic acid inhibits fibroblast proliferation after glaucoma filtration surgery.

Mammalian cells in culture have individual nutritional requirements which are mainly fulfilled by the addition of fetal calf serum to the basic culture medium. Since many of the serum components are as yet poorly understood or even completely unknown, a number of difficulties arise in the evaluation of the effect of exogenously added factors or drugs on the growth of the cells. This paper presents data demonstrating the successful adaptation, routine cultivation and cryopreservation of bovine lens epithelial cells (BLEC) under serum-free culture conditions by use of the commercially available serum substitutes BMS, BM 86 Wissler and Ultroser G. Moreover, a culture medium especially designed for cell quiescence, named LR-1, is presented. Cells cultivated in culture medium containing 10% fetal calf serum served as controls. While BM-86 Wissler caused significantly reduced growth rates within 2 days and, finally, cell death after 12 days of incubation, the use of BMS resulted in growth rates which did not differ from the corresponding controls. Ultroser G resulted in a significant increase of proliferative activity of BLEC. LR-1 medium caused cell quiescence and kept the cells alive for a number of days. Thus, LR-1 allowed evaluation of the response of the cells to a mitogenic mixture from bovine brain mainly containing endothelial cell growth factor. The results demonstrate that cultivation of BLEC is possible under serum-free culture conditions. Moreover, the medium LR-1, which causes cell quiescence, is useful for the evaluation of growth factor-induced effects in vitro.

Reaction of the cyclic amides EN^tBuSiMe2N^tBu (E = Ge, Sn) with the heterobimetallic complexes [(OC)3Fe(μ-CO)(μ-Ph2PXPPh2)Pt(PR3)](Fe−Pt) (X = CH2, NH; R = phenyl, p-tolyl) occurs by selective substitution of the bridging carbonyl ligand and yields the stannylene- and germylene-bridged complexes [(OC)3Fe{μ-EN^tBuSiMe2N^tBu}(μ-Ph2PXPPh2)Pt(PR3)](Fe−Pt) (2a, X = CH2, E = Sn, R = Ph; 2b, X = NH, E = Sn, R = Ph; 2c, X = CH2, E = Sn, R = p-tol; 3a, X = CH2, E = Ge, R = Ph; 3b, X = NH, E = Ge, R = Ph). When GeN^tBuSiMe2N^tBu was added in excess to the germylene complex 3a, the tetranuclear complex [(OC)3Fe{μ-GeN^tBuSiMe2N^tBu}(μ-dppm)Pt {GeN^tBuSiMe2N^tBu}](Fe−Pt) (4) was formed, which is in equilibrium with 3a. The heterobimetallic Si(OMe)3-substituted complexes mer-[(OC)3Fe{μ-Si(OMe)2(OMe)}(μ-dppm)M(Me)](Fe−M) (M = Pd, Pt) react with EN^tBuSiMe2N^tBu (E = Ge, Sn) by opening of the four-membered Fe−Si−O−M ring to give the complexes mer-[(OC)3Fe{μ-Si(OMe)2(OMe)}{EN^tBuSiMe2N^tBu}{μ-dppm)M}(Me)](Fe−M) (5, M = Pt, E = Sn; 6, M = Pd, E = Sn; 7, M = Pd, E = Ge) which contain a five-membered Fe−Si−O−E−M ring. The expected insertion of the amides EN^tBuSiMe2N^tBu into the M−Me bond was not observed. The dynamic behavior of these intramolecularly base-stabilized trimetallic germylene and stannylene complexes, which is due to a rapid exchange of the methoxy groups coordinated on E, was investigated by variable-temperature ¹H-NMR spectroscopy. All complexes were characterized by multinuclear NMR spectroscopy, and the solid-state structure of 7 was determined by X-ray diffraction.

Abstract: · Background: In order to develop new strategies for the pharmacological modulation of posttraumatic and postsurgical wound healing of the corneal stroma, the effect of Trapidil, a competitive platelet-derived growth factor (PDGF) antagonist, on the proliferation of cultured bovine stromal fibroblasts (BSF) was investigated. · Methods: BSF, obtained from explant cultures, were seeded at a cell density of 100/mm2. The effect of various concentrations of Trapidil on cell viability and cell proliferation was determined using three different culture conditions: (1) serum-free medium (WM/F12), (2) serum-containing medium (WM/F12+10% FCS), and (3) serum-free medium +50 ng/ml PDGF-BB. Trapidil was added in concentrations ranging from 100 μg/ml to 400 μg/ml. Cell numbers were determined 2 and 5 days after addition of Trapidil, using a computer-based cell-counting system. Cell viability was evaluated morphologically and by means of a repopulation assay. · Results: Addition of Trapidil (100–400 μg/ml) led to a significant, dose-dependent inhibition of both serum- and PDGF-BB-induced proliferation of BSF. In contrast, treatment of quiescent BSF, cultured in serum-free medium, did not result in a significant reduction of cell number. No cytotoxic effects were observed. · Conclusion: The results of the present study demonstrate an inhibitory effect of Trapidil on the proliferation of BSF. It can be assumed that application of Trapidil might be a useful tool in the prevention of corneal complications after trauma (e.g., scarring, astigmatism and – with respect to photorefractive procedures – formation of haze and regression of the refractive effect).

Ohne Zusammenfassung:

Ohne Zusammenfassung:

Sans rsum:

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

The attempted CO/phosphine exchange reaction of the hydrido(silyl)tetracarbonyl‐Fe complexes (I) with the diphosphine (II) results in the unexpected formation of the dihydride complex (III).

The phosphane‐substituted anionic silyl complexes (II) prepared from (I) are distinctly more reactive than their tetracarbonyl analogues, particularly towards metal or metal‐complex halides.

The complexes (I), (II), and (III) are synthesized by several routes shown by examples: by photochemical reaction of dppe‐substituted Fe carbonyl with silanes, by thermal reaction of (OC)4Fe(SiR3)2or (OC)4Fe(H)SiR3with dppe, or by exchange of the silyl groups.

The diphosphine‐ and O‐Si‐bridged dinuclear complexes (III) are obtained according to the scheme.