Longitudinal Spin Fluctuations Driving Field-Reinforced Superconductivity in UTe_{2}.

Our measurements of ^{125}Te NMR relaxations reveal an enhancement of electronic spin fluctuations above µ_{0}H^{*}∼15 T, leading to their divergence in the vicinity of the metamagnetic transition at µ_{0}H_{m}≈35 T, below which field-reinforced superconductivity appears when a magnetic field (H) is applied along the crystallographic b axis. The NMR data evidence that these fluctuations are dominantly longitudinal, providing a key to understanding the peculiar superconducting phase diagram in H∥b, where such fluctuations enhance the pairing interactions.

Terahertz phase contrast imaging of sorption kinetics in porous coordination polymer nanocrystals using differential optical resonator.

The enhancement of light-matter coupling when light is confined to wavelength scale volumes is useful both for studying small sample volumes and increasing the overall sensing ability. At these length scales, nonradiative interactions are of key interest to which near-field optical techniques may reveal new phenomena facilitating next-generation material functionalities and applications. Efforts to develop novel chemical or biological sensors using metamaterials have yielded innovative ideas in the optical and terahertz frequency range whereby the spatially integrated response over a resonator structure is monitored via the re-radiated or leaked light. But although terahertz waves generally exhibit distinctive response in chemical molecules or biological tissue, there is little absorption for subwavelength size sample and therefore poor image contrast. Here, we introduce a method that spatially resolves the differential near-field phase response of the entire resonator as a spectral fingerprint. By simultaneously probing two metallic ring resonators, where one loaded with the sample of interest, the differential phase response is able to resolve the presence of guest molecules (e.g. methanol) as they are adsorbed or released within the pores of a prototypical porous coordination polymer.

Ferromagnetic quantum critical point in heavy-fermion iron oxypnictide Ce(Ru(1-x)Fe(x))PO.

We have performed (31)P-NMR measurements on Ce(Ru(1-x)Fe(x))PO in order to investigate ferromagnetic (FM) quantum criticality, since a heavy-fermion (HF) ferromagnet CeRuPO with a two-dimensional structure turns into a HF paramagnet by an isovalent Fe substitution for Ru. We found that Ce(Ru(0.15)Fe(0.85))PO shows critical fluctuations down to ~0.3 K, as well as the continuous suppression of Curie temperature and the ordered moments by the Fe substitution. These experimental results suggest the presence of a FM quantum critical point (QCP) at x~0.86, which is a rare example among itinerant ferromagnets. In addition, we point out that the critical behaviors in Ce(Ru(0.15)Fe(0.85))PO share a similarity with those in YbRh(2)Si(2), where the local criticality of f electrons has been discussed. We reveal that Ce(Ru(1-x)Fe(x))PO is a new system to study FM quantum criticality in HF compounds.

Superconducting spin smecticity evidencing the Fulde-Ferrell-Larkin-Ovchinnikov state in Sr2RuO4.

Translational symmetry breaking is antagonistic to static fluidity but can be realized in superconductors, which host a quantum-mechanical coherent fluid formed by electron pairs. A peculiar example of such a state is the Fulde-Ferrell-Larkin-Ovchinnikov (FFLO) state, induced by a time-reversal symmetry-breaking magnetic field applied to spin-singlet superconductors. This state is intrinsically accompanied by the superconducting spin smecticity, spin density-modulated fluidity with spontaneous translational-symmetry breaking. Detection of such spin smecticity provides unambiguous evidence for the FFLO state, but its observation has been challenging. Here, we report the characteristic "double-horn" nuclear magnetic resonance spectrum in the layered superconductor Sr2RuO4 near its upper critical field, indicating the spatial sinusoidal modulation of spin density that is consistent with superconducting spin smecticity. Our work reveals that Sr2RuO4 provides a versatile platform for studying FFLO physics.

Charge-neutral fermions and magnetic field-driven instability in insulating YbIr3Si7.

Kondo lattice materials, where localized magnetic moments couple to itinerant electrons, provide a very rich backdrop for strong electron correlations. They are known to realize many exotic phenomena, with a dramatic example being recent observations of quantum oscillations and metallic thermal conduction in insulators, implying the emergence of enigmatic charge-neutral fermions. Here, we show that thermal conductivity and specific heat measurements in insulating YbIr3Si7 reveal emergent neutral excitations, whose properties are sensitively changed by a field-driven transition between two antiferromagnetic phases. In the low-field phase, a significant violation of the Wiedemann-Franz law demonstrates that YbIr3Si7 is a charge insulator but a thermal metal. In the high-field phase, thermal conductivity exhibits a sharp drop below 300 mK, indicating a transition from a thermal metal into an insulator/semimetal driven by the magnetic transition. These results suggest that spin degrees of freedom directly couple to the neutral fermions, whose emergent Fermi surface undergoes a field-driven instability at low temperatures.

Metamagnetic behavior and Kondo breakdown in heavy-fermion CeFePO.

We report that nonmagnetic heavy-fermion (HF) iron oxypnictide CeFePO with two-dimensional XY-type anisotropy shows a metamagnetic behavior at the metamagnetic field H(M)≃4 T perpendicular to the c axis and that a critical behavior is observed around H(M). Although the magnetic character is entirely different from that in other Ce-based HF metamagnets, H(M) in these metamagnets is linearly proportional to the inverse of the effective mass, or to the temperature where the susceptibility shows a peak. This finding suggests that H(M) is a magnetic field breaking the local Kondo singlet, and the critical behavior around H(M) is driven by the Kondo breakdown accompanied by the Fermi-surface instability.

Induction of anti-allo-class I H-2 tolerance by inactivation of CD8+ helper T cells, and reversal of tolerance through introduction of third-party helper T cells.

The intravenous sensitization of C57BL/6 (B6) mice with class I H-2-disparate B6-C-H-2bm1 (bm1) spleen cells resulted in the abrogation of CD8+ T cell-mediated anti-bm1 (proliferative and interleukin 2-producing) T helper (Th) cell activities. In vitro stimulation of lymphoid cells from these mice with bm1 cells, however, generated a reduced, but appreciable, anti-bm1 cytotoxic T lymphocyte (CTL) response. Moreover, the anti-bm1 CTL response, upon stimulation with [bm1 x B6-C-H-2bm12 (bm12)]F1 spleen cells, was enhanced when compared with the response induced upon stimulation with bm1 cells. These in vitro results were reflected on in vivo graft rejection responses; bm1 skin grafts engrafted in the bm1-presensitized B6 mice exhibited prolonged survival, whereas (bm1 x bm12)F1 grafts placed collateral to bm1 grafts (dual engrafted mice) inhibited the tolerance to bm1. In the B6 mice 1-2 d after rejecting the bm1 grafts, anti-bm1 Th activities remained marginal, whereas potent anti-bm1 CTL responses were found to be generated from their spleen cells. Administration in vivo of anti-CD4 antibody into bm1-presensitized, dual graft-engrafted mice prolonged bm1 graft survival and interfered with enhanced induction of anti-bm1 CTL activity. These results indicate that anti-class I alloantigen (bm1) tolerance as induced by intravenous presensitization with the relevant antigens is not ascribed to the elimination of CD8+ CTL precursors, but to the specific inactivation of CD8+ Th cells, whose function can be bypassed by activating third-party Th cells.

Cell-cell interaction in graft rejection responses: induction of anti-allo-class I H-2 tolerance is prevented by immune responses against allo-class II H-2 antigens coexpressed on tolerogen.

The intravenous sensitization of C57BL/6 (B6) mice with class I H-2-disparate B6-C-H-2bm1 (bm1) spleen cells results in almost complete abrogation of anti-bm1 CD8+ helper (proliferative and interleukin 2-producing) T cell (Th) activities. Although an appreciable portion of CD8+ cytotoxic T lymphocyte (CTL) precursors themselves remained after this regimen, such a residual CTL activity was eliminated after the engrafting of bm1 grafts, and these grafts exhibited prolonged survival. In contrast, the intravenous sensitization with (bm1 x B6-C-H-2bm12 [bm12])F1 cells instead of bm1 cells failed to induce the prolongation of bm1 graft survival as well as bm12 and (bm1 x bm12)F1 graft survival. In the (bm1 x bm12)F1-presensitized B6 mice before as well as after the engrafting of bm1 grafts, anti-bm1 CTL responses that were comparable to or slightly stronger than those observed in unpresensitized mice were induced in the absence of anti-bm1 Th activities. bm1 graft survival was also prolonged by intravenous presensitization with a mixture of bm1 and bm12 cells but not with a mixture of bm1 and (bm1 x bm12)F1 cells. The capacity of CD4+ T cells to reject bm12 grafts was eliminated by intravenous presensitization with antigen-presenting cell (APC)-depleted bm12 spleen cells. However, intravenous presensitization with APC-depleted (bm1 x bm12)F1 cells failed to induce the prolongation of bm1 graft survival under conditions in which appreciably prolonged bm12 graft survival was induced. More surprisingly, bm1 graft survival was not prolonged even when the (bm1 x bm12)F1 cell presensitization was performed in CD4+ T cell-depleted B6 mice. This contrasted with the fact that conventional class I-disparate grafts capable of activating self Ia-restricted CD4+ as well as allo-class I-reactive CD8+ Th exhibited prolonged survival in CD4+ T cell-depleted, class I-disparate cell-presensitized mice. These results indicate that: (a) intravenous presensitization with class I- and II-disparate cells fails to reduce anti-allo-class I rejection responses that would otherwise be eliminated using only class I-disparate cells; (b) such failure is generated according to the coexpression of both classes of alloantigens on a single cell as tolerogen; and (c) allo-class II antigens coexpressed on tolerogen function to activate CD4+ as well as non-CD4+ Th leading to the generation of anti-class I effector T cell responses.

Heterogenous graft rejection pathways in class I major histocompatibility complex-disparate combinations and their differential susceptibility to immunomodulation induced by intravenous presensitization with relevant alloantigens.

The present study investigates the heterogeneity of graft rejection pathways in class I major histocompatibility complex (MHC)-disparate combinations and the susceptibility of each pathway to immunomodulation induced by intravenous presensitization with alloantigens. Depletion of CD8+ T cells was induced by repeated administration of anti-CD8 monoclonal antibody. CD8+ T cell-depleted mice failed to generate anti-allo class I MHC cytotoxic T cell (CTL) responses but exhibited anti-allo class I MHC T cell responses, such as mixed lymphocyte reaction (MLR)/IL-2 production, that were induced by CD4+ T cells. In contrast, donor-specific intravenous presensitization (DSP), as a model of donor-specific transfusion, induced almost complete elimination of CD4+ and CD8+ T cell-mediated MLR/IL-2 production, whereas this regimen did not affect the generation of CTL responses induced by DSP-resistant elements (CD8+ CTL precursors and CD4+ CTL helpers). Prolongation of skin graft survival was not induced by either of the above two regimens alone, but by the combination of these. Prolonged graft survival was obtained irrespective of whether the administration of anti-CD8 antibody capable of eliminating CTL was started before or after DSP. The combination of DSP with injection of anti-CD4 antibody also effectively prolonged graft survival. However, this was the case only when the injection of antibody was started before DSP, because such antibody administration was capable of inhibiting the generation of CTL responses by eliminating DSP-resistant CD4+ CTL helpers. These results indicate that (a) the graft rejection in class I-disparate combinations is induced by CD8+ CTL-involved and -independent pathways that are resistant and susceptible to DSP, respectively; (b) DSP contributes to, but is not sufficient for, the prolongation of graft survival; and (c) the suppression of graft rejection requires an additional treatment for reducing DSP-resistant CTL responses. The results are discussed in the context of potential clinical application in attempts to inhibit the generation of DSP-resistant CTL responses upon the prospective DSP.

Characterization of the 4C8 antigen involved in transendothelial migration of CD26(hi) T cells after tight adhesion to human umbilical vein endothelial cell monolayers.

In extravasation of T cells, little is known about the mechanisms of transendothelial migration subsequent to the T cells' tight adhesion to endothelium. To investigate these mechanisms, we developed a monoclonal antibody (mAb), termed anti-4C8, that blocks transmigration but not adhesion in a culture system in which high CD26-expressing (CD26(hi)) T cells preferentially migrate through human umbilical vein endothelial cell (HUVEC) monolayers cultured on collagen gels. Anti-4C8 reacted with all CD3(+) T cells and monocytes but not neutrophils or HUVECs. The structure defined by this antibody was an 80-kD molecule. The mAb at 1 mug/ml inhibited 80-90% of migration of CD3(+) T cells through unstimulated and interferon gamma-stimulated HUVEC monolayers without interfering with adhesion and cell motility. When added to the cultures after the adhesion, anti-4C8 completely blocked subsequent transmigration of adherent T cells. Phase-contrast and electron microscopy revealed that T cells are arrested at the intercellular junctions of HUVECs in the presence of anti-4C8. Anti-4C8 exhibited agonistic effects on resting T cells without other stimuli under culture conditions in which anti-4C8 can stimulate T cells. First, in the checkerboard assay using collagen gels, the antibody promoted chemokinetic migration of the cells in a dose-dependent manner from 0.1 to 10 mug/ml. The predominant population of T cells that migrated into collagen gels with impregnated anti-4C8 were CD26(hi). Second, solid-phase-immobilized anti-4C8 induced adhesion of T cells to the substrate, often with polarizations in cell shape and large pseudopods rich in filamentous (F-) actin. Third, soluble anti-4C8 augmented F-actin content preferentially in CD26(hi) T cells when added to T cells at a high dose of 10 mug/ml. Finally, both anti-4C8-induced chemokinetic migration and transendothelial migration were inhibited by pretreatment of T cells with pertussis toxin. These findings suggest that stimulation via the 4C8 antigen increases cell motility of CD26(hi) cells with profound cytoskeletal changes through signaling pathways including G proteins. The 4C8 antigen may be involved in preferential transmigration of CD26(hi) cells adherent to HUVECs.

Unconventional superconductivity and antiferromagnetic quantum critical behavior in the isovalent-doped BaFe2(As1-xPx)2.

Spin dynamics evolution of BaFe2(As(1-x)Px){2} was probed as a function of P concentration via 31P NMR. Our NMR study reveals that two-dimensional antiferromagnetic (AF) fluctuations are notably enhanced with little change in static susceptibility on approaching the AF phase from the superconducting dome. Moreover, the magnetically ordered temperature θ deduced from the relaxation rate vanishes at optimal doping. These results provide clear-cut evidence for a quantum-critical point, suggesting that the AF fluctuations associated with the quantum-critical point play a central role in the high-T(c) superconductivity.

Electron microscopic investigations of actomyosin as a function of ionic strength.

Natural actomyosin at micro = 0.6 appears in various forms, including the regular arrowhead structures originally reported by Huxley (1), when it has been stained negatively with 1% uranyl acetate. In addition to the arrowheads, thin whiskers, 700-1200 A in length and 20 A in width, attached to the arm of the arrowheads have been demonstrated. The dimensions of the whiskers and arms of the arrowheads are practically the same as those of the light meromyosin (LMM) and the heavy meromyosin (HMM) moieties of the single myosin molecule, respectively. Changes in the electron microscopically distinguishable elements during aggregation of natural actomyosin on reduction of the ionic strength have been observed. At micro = 0.4, partial aggregation of the LMM whiskers begins to result in some parallel alignment of the arrowhead-bearing filaments (acto-HMM). In the range of micro = 0.3-0.1, the LMM whiskers merge into smooth filaments which are arranged alternatingly with arrowhead-bearing filaments. Thus, lateral aggregation of composite actomyosin filaments (acto-HMM + LMM whiskers) results with the LMM moieties as links. This view is supported by the following facts: (a) acto-HMM is devoid of whiskers and does not show lateral aggregation at micro = 0.1; (b) natural actomyosin digested with trypsin at micro = 0.6, which was followed by removal of LMM aggregates at low ionic strength, is essentially the same as acto-HMM at micro = 0.1; and (c) digestion with trypsin of natural actomyosin at micro = 0.2 for varying periods of time leads to a separation of arrowhead-bearing filaments from LMM aggregates.

Effects of intracerebroventricular administration of neuromedin U or neuromedin S in steers.

Although neuromedin U (NMU) and neuromedin S (NMS) are reported to modulate stress responses mainly through corticotropin-releasing hormone system in rodents, the in vivo effects of centrally administered NMU or NMS on stress regulation have not been fully elucidated in cattle. We examined adrenocorticotropic hormone levels, body temperature, and behavioral responses to intracerebroventricularly (ICV) administered rat NMU or rat NMS in steers. ICV NMU and NMS (0.2, 2, and 20 nmol/200 microl) evoked a dose-related increase in plasma cortisol concentrations (CORT). There was a significant time-treatment interaction for the time course of CORT (p<0.001). ICV NMU evoked a dose-related increase in rectal temperature (RT). There was a significant time-treatment interaction for the change in RT from pre-injection value (p<0.05). There was a significant difference among treatments in the percentage of time spent lying (Friedman's test, chi(2)=15.6, p<0.01) and in the total number of head shaking (Friedman's test, chi(2)=14.49, p<0.01). A high dose of NMS tended to shorten the duration of lying and increase the number of head shaking. These findings indicate that both central NMU and NMS might participate in controlling the hypothalamo-pituitary-adrenal axis, that central NMU might participate in controlling body temperature, and that central NMS is likely to be involved in behavioral activation in cattle.

Increased basal phosphorylation of mitogen-activated protein kinases and reduced responsiveness to inflammatory cytokines in neutrophils from patients with rheumatoid arthritis.

OBJECTIVE: We studied the functions of peripheral blood (PB) and synovial fluid (SF) neutrophils from patients with rheumatoid arthritis (RA), focusing the molecular basis for the activated state and the functional responsiveness of RA neutrophils to inflammatory cytokines. METHODS: Paired samples of PB neutrophils and SF neutrophils from the inflamed knee joint were obtained from 18 RA patients (5 males and 13 females). RESULTS: RA neutrophils exhibited increased spontaneous superoxide (O2-) release and adherence, increased basal phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase, accelerated spontaneous apoptosis, and enhanced O2- release in response to N-formyl-methionyl-leucyl-phenylalanine as compared with healthy normal PB neutrophils. When challenged with granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF) or tumor necrosis factor alpha (TNF-alpha), RA neutrophils exhibited reduced responses to these cytokines, which included O2- release, adherence, priming for enhanced O2- release, and phosphorylation of ERK and p38. The functional alterations were greater in SF neutrophils than in PB neutrophils from RA. Reduced responsiveness to cytokines in RA neutrophils was closely associated with increased serum and SF levels of GM-CSF and TNF-alpha. RF and RAHA titers were closely correlated with increased TNF-alpha level in SF. CONCLUSION: These findings indicate that RA neutrophils are in the activated state with increased basal phosphorylation of ERK and p38, and exhibit reduced responsiveness to inflammatory cytokines (G-CSF, GM-CSF and TNF-alpha) and accelerated spontaneous apoptosis.

Method development and validation for the simultaneous determination of cinnarizine and co-formulated drugs in pharmaceutical preparations by capillary electrophoresis.

Rapid and simple capillary electrophoresis (CE) methods were developed for the simultaneous determinations of cinnarizine and domperidone (CN/DOM) and cinnarizine and nicergoline (CN/NIC) in their co-formulated tablets. The optimized CE conditions were as follows: running buffer, methanol-acetate buffer (pH 3.0, 10 mM) (80:20 and 85:15 (v/v) for CN/DOM and CN/NIC, respectively); applied voltage, 20 kV; UV detection wavelengths, 215 and 227 nm for CN/DOM and CN/NIC, respectively; hydrodynamic injection was performed at a height of 25 mm for 30 s. Quinine hydrochloride and nicardipine hydrochloride were used as internal standards for the determination of CN/DOM and CN/NIC, respectively. Calibration curves were linear over the ranges 0.25-20/0.375-15 microg/ml (CN/DOM) and 0.25-25/0.4-10 microg/ml (CN/NIC) in each optimized condition. Detection limits were 0.074/0.119 microg/ml and 0.072/0.116 microg/ml for CN/DOM and CN/NIC, respectively. The proposed methods were successfully applied for the simultaneous determination of both CN/DOM and CN/NIC in their co-formulated tablets without interfering peaks due to the excipients present in the pharmaceutical tablets. The estimated amounts of CN/DOM and CN/NIC were almost identical with the certified values, and their percentage relative standard deviation values (%R.S.D.) were found to be < or =2.34% (n=3).

Evidence that proteases are involved in superoxide production by human polymorphonuclear leukocytes and monocytes.

The possible participation of proteases in superoxide (O2-) production by human polymorphonuclear leukocytes (PMN) and monocytes was explores using various protease inhibitors and substrates. Protease inhibitors of serine proteases and synthetic inhibitors that modify the active site of serine proteases. Substrates used were synthetic substrates of the chymotrypsin type as well as trypsin type of protease. All these inhibitors and substrates inhibited O2- oroduction by human PMN and monocytes induced by cytochalasin E and concanavalin A, though PMN were more sensitive to these inhibitors and substrates than monocytes. Inhibition appeared rapidly even when the inhibitors were added at the same time as the stimulants, during the "induction time of O2-production" or at the time of maximum O2- production, whereas much greater inhibition was observed when the cells were preincubated with the inhibitors. These observations suggest that enzymatically active serine proteases are essential for these phagocytic cells to initiate and maintain the O2- production in response to the stimuli. The inhibitory effect of the inhibitor and substrate for chymotrypsin type protease was greater than that of those substances for trypsin-type protease. Macromolecular inhibitors also inhibited the O2- production. These findings suggest that the serine proteases involved in the O2- production by human PMN and monocytes are similar to chymotrypsin rather than trypsin, and are possibly located at the cell surface membrane.

Functional maturation of membrane potential changes and superoxide-producing capacity during differentiation of human granulocytes.

The alterations of stimulus-induced membrane potential changes, superoxide (O2-)-producing capacity and phagocytic activity during differentiation of human granulocytes were investigated in the human leukemia cell lines HL-60 and KG-1 differentiating in vitro and in human leukemic granulocytes obtained from chronic myelogenous leukemia patients. HL-60 cells incubated with dimethyl sulfoxide or with retinoic acid showed progressively increasing O2- production as well as membrane potential changes (depolarization) on contact with phorbol myristate acetate or the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine, with a concomitant increase in the proportion of mature cells of the granulocytic type. Phagocytosis of latex particles, yeast, and oil droplets appeared 24 h after incubation with dimethyl sulfoxide and anteceded the increment of O2- production and membrane potential changes, both of which appeared concomitantly 3 d after incubation with dimethyl sulfoxide. Similar findings were observed when immature and mature granulocytes obtained from chronic myelogenous leukemia patients were stimulated by phorbol ester, the chemotactic peptide, or calcium ionophore A23187, and the amount of O2- production was parallel to the magnitude of membrane potential changes. HL-60 and KG-1 cells incubated for 1-6 d with phorbol myristate acetate showed neither O2- production nor membrane potential changes on contact with phorbol ester, chemotactic peptide, or A23187, although such cells resembled macrophages morphologically, and their phagocytic activity was significantly increased. O2- production and membrane potential changes in normal granulocytes induced by phorbol ester, chemotactic peptide and A23187 were inhibited by 2-deoxyglucose. These findings indicate that the O2--producing system and the system provoking membrane potential changes may develop concomitantly as human granulocytes mature and differentiate, and that the development of these systems and of phagocytic activity may be independently regulated.

Characteristics of periodontal ligament subpopulations obtained by sequential enzymatic digestion of rat molar periodontal ligament.

Periodontal ligament (PDL) consists of different cell populations in various differentiation stages. In the present study, we isolated cell populations from rat molar PDL by sequential enzymatic digestion and characterized growth potential and mineralization activity of the PDL subpopulations (PDL-SP) to throw light on the mechanism of PDL remodeling and, in its turn, periodontal tissue regeneration. PDL attached to extracted rat molars was digested 2 mg/ml collagenase and 0.25% trypsin at 37 degrees C for 30 min. Then four consecutive digestions were performed for 20 min each in a fresh digestive solution. The solutions were centrifuged to collect released cells and 5 PDL subpopulations (30M-, 50M-, 70M-, 90M-and 110M-PDL-SP) were obtained. Light microscopic observation showed that about a half of PDL in width attached on the root surface of extracted teeth and 30M-PDL-SP was considered to contain cells mainly from middle portion of PDL. Scanning electron microscopic examination indicated that 110M-PDL-SP was enriched by root lining cementoblastic cells. 30M-PDL-SP showed a high level of proliferative activity. Although the growth potential of a subpopulation decreased in PDL-SP toward the root surface, 110M-PDL-SP had a high proliferative activity equivalent to that of 30M-PDL-SP. Analyses of alkaline phosphatase (ALP) and mineralization activities showed that higher activities in PDL-SP toward the surface of roots and that 110M-PDL-SP had the highest activity of ALP and the largest number of mineralization nodules. The present study shows as supposed by previous studies on cell kinetics in PDL that subpopulations with larger growth potential were generally located in the middle portion of PDL and those with higher mineralization activities toward the surface of the roots. It is suggested, however, that a possible pathway of PDL cell turnover may exist within the PDL-SP on the root surface in addition to the generally recognized pathway from the middle area of PDL to root surface.

Activation of human neutrophil by cytokine-activated endothelial cells.

Cytokine activation of vascular endothelial cells renders the hyperadhesiveness for neutrophils. During the processes of inflammation and atherosclerosis, the production of reactive oxygen species by neutrophils contributes to endothelial cell (EC) damage and injury. However, the precise mechanisms for neutrophil activation by ECs remain unknown. Thus, we investigated what kinds of pathophysiological factors synthesized by inflammatory cytokine-activated ECs potentiated the activity of neutrophil functions. The magnitude of O(2)(-) release from neutrophils, which is one of pivotal neutrophil functions, was measured as an indicator potentiated by activated ECs. Neutrophils release massive amounts of O(2)(-) on coculture with activated ECs. Anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibody (Ab) or specific platelet-activating factor (PAF)-receptor antagonist suppressed the O(2)(-) release from neutrophils on coculture with the activated ECs by 50% to 70%. The supernatants from activated ECs also induced O(2)(-) release by neutrophils. This stimulatory effect of activated EC supernatants on O(2)(-) release by neutrophils was abolished by anti-GM-CSF Ab or by PAF-receptor antagonist. As we previously reported, we demonstrated the expression of GM-CSF mRNA by Northern blotting and protein synthesis of GM-CSF by ELISA on tumor necrosis factor as well as interleukin-1-activated ECs. Although phosphorylation of mitogen-activated protein kinases was observed in ECs stimulated by tumor necrosis factor and interleukin-1, treatment of ECs with PD98059 (MEK1 inhibitor) and SB203580 (p38 mitogen-activated protein kinase inhibitor) in the presence of the cytokine failed to attenuate the stimulatory effect of activated ECs on neutrophil activation. We found that activated ECs regulated neutrophil function on coculture. We show here for the first time, to our knowledge, that the collaboration between GM-CSF and PAF synthesized by activated ECs markedly potentiated neutrophil activation.

Freeze-drying synthesis of an amorphous Zn(2+) complex and its transformation to a 2-D coordination framework in the solid state.

An amorphous and metastable precursor for a Zn two-dimensional coordination framework was synthesised via freeze drying. The precursor comprises randomly packed discrete clusters of a Zn complex. The amorphous-to-crystalline framework transformation, which was triggered by the gentle application of heat or pressure, was accompanied by a change in the coordination geometry of the Zn(2+) ions from tetrahedral to octahedral symmetry.