Effects of parecoxib on postoperative cognitive dysfunction and serum levels of NSE and S100ß in elderly patients undergoing surgery.

OBJECTIVE: To investigate the effects of parecoxib on postoperative cognitive dysfunction, and serum levels of neuron-specific enolase (NSE) and S100ß protein (S100ß) in elderly patients undergoing surgery. PATIENTS AND METHODS: The retrospective cohort study method was used to collect the clinical data of 94 elderly patients who underwent elective orthopedic and general anesthesia surgery in our hospital from September 2020 to February 2022. 94 patients were divided into the control group (47 cases) and the study group (47 cases), according to different intervention methods. In the study group, 40 mg of parecoxib was injected intravenously into patients 30 min before the induction of anesthesia, and the patients in the control group were given the same dose of normal saline intravenously before the operation. The basic clinical data of the patients were collected. The levels of the indexes before operation and 6 hours after operation were compared between the two groups, including the Montreal Cognitive Scale (MoCA) score, inflammatory factor indicators [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), interleukin-10 (IL-10), interleukin-1ß (IL-1ß), monocyte chemokine-1 (MCP-1), and inducible nitric oxide synthase (iNOS)], serum cortisol (CORT), beta-amyloid (ß-AP), adiponectin (ADP), NSE, and S100ß. RESULTS: No significant differences in the preoperative MoCA score, TNF-α, IL-6, CRP, IL-10, IL-1ß, MCP-1, iNOS, CORT, ß-AP, ADP, NSE, and S100ß levels were observed between the two groups (p>0.05). The postoperative MoCA score in the study group was significantly higher than that in the control group (p<0.05). The postoperative levels of TNF-α, IL-6, CRP and IL-1ß in the study group were significantly lower than those in the control group (p<0.05), and the postoperative levels of IL-10, MCP-1 and iNOS in the study group were significantly higher than those in the control group (p<0.05). CONCLUSIONS: Parecoxib can notably inhibit the levels of postoperative inflammatory cytokines, improve neurological dysfunction, and reduce the occurrence of postoperative cognitive dysfunction in patients. The contents of serum NSE and S100ß have potential value in the diagnosis of postoperative cognitive dysfunction in elderly patients.

Continuous wave dual-wavelength Nd:YVO4 laser at 1342 and 1525†nm for generating a 714-nm emission.

Continuous wave dual-wavelength lasers at 1342 and 1525 nm are developed by using separate Nd:YVO4 and YVO4 crystals to form compactly coupled cavities for fundamental and Raman waves, respectively. The design of the coupled cavity not only reduces the thermal lensing effect in the Nd:YVO4 crystal, but also improves the stimulated Raman scattering (SRS) efficiency in the undoped YVO4 crystal. In addition, the Raman crystal is coated to form a highly reflective mirror to minimize cavity losses. By using a plano-concave cavity with a pump power of 40 W, the output powers of the fundamental and Raman waves are 470 mW and 310 mW, respectively. Changed to a concave cavity, the output powers of fundamental and Raman waves are 220 mW and 510 mW, respectively. Basis on the dual-wavelength operation, the maximum output power at 714 nm can reach 2.0 W via the sum frequency generation. A light source at 714 nm can be used for laser spectroscopy of atomic and ionic radium isotopes.

Role of transient receptor potential vanilloid 1 in regulating erythropoietin-induced activation of endothelial nitric oxide synthase.

AIMS: Erythropoietin (EPO), the key hormone involved in erythropoiesis, beneficially affects endothelial cells (ECs), but the detailed mechanisms are yet to be completely understood. In this study, we investigated the role of transient receptor potential vanilloid type 1 (TRPV1), a ligand-gated non-selective calcium (Ca2+ ) channel, in EPO-mediated endothelial nitric oxide synthase (eNOS) activation and angiogenesis. METHODS AND RESULTS: In ECs, EPO time dependently increased intracellular levels of calcium; this increase was abrogated by the Ca2+ chelators and pharmacological inhibitors of TRPV1 in bovine aortic ECs (BAECs) and TRPV1-transfected HEK293 cells. In addition, EPO-induced nitrite oxide (NO) production, phosphorylation of eNOS, Akt and AMP-activated protein kinase (AMPK) and the formation of TRPV1-Akt-AMPK-eNOS complex as well as tube formation were diminished by the pharmacological inhibition of TRPV1 in BAECs. Moreover, EPO time dependently induced the phosphorylation of phospholipase C-γ1 (PLC-γ1). Inhibition of PLC-γ1 activity blunted the EPO-induced Ca2+ influx, eNOS phosphorylation, TRPV1-eNOS complex formation and NO production. The phosphorylated level of eNOS increased in the aortas of EPO-treated wild-type (WT) mice or EPO-transgenic (Tg) mice but not in those of EPO-treated TRPV1-deficient (TRPV1-/- ) mice or EPO-Tg/TRPV1-/- mice. Matrigel plug assay showed that EPO-induced angiogenesis was abrogated in TRPV1 antagonist capsazepine-treated WT mice and TRPV1-/- mice. CONCLUSION: These findings indicate the EPO-induced Ca2+ influx via the activation of the PLC-γ1 signalling pathway, which leads to TRPV1 activation and consequently increases the association of the TRPV1-Akt-AMPK-eNOS complex, eNOS activation, NO production and angiogenesis.

Synthesis of carbonated hydroxyapatite nanospheres through nanoemulsion.

This study investigated the nanoemulsion technique as a means to synthesize carbonated hydroxyapatite (CHAp) nanospheres which could be used to produce composite tissue engineering scaffolds. CHAp nanospheres were successfully synthesized by mixing an acetone solution of Ca(NO(3))(2).4H(2)O with an aqueous solution of (NH(4))(2)HPO(4) and NH(4)HCO(3). Four reaction temperatures, namely, 4, 25, 37 and 55 degrees C, were investigated and no surfactant was added in all nanoemulsion processes. Wet slurries of CHAp from the nanoemulsions were freeze-dried to obtain dry powders. X-ray diffraction (XRD) results showed that the as-synthesized CHAp nanoparticles were mainly in an amorphous state. After calcination at 900 degrees C, the apatite became well crystallized. Fourier transform infrared (FTIR) spectroscopy showed that the CHAp was B-type substitution. Both scanning electron microscopy (SEM) and transmission electron microscopy (TEM) revealed that the CHAp particles were spherical in shape and that their sizes were in the nanometer range. The successful synthesis of CHAp nanospheres is a critical step forward in our efforts to fabricate bone tissue engineering scaffolds using the selective laser sintering technology.

Anti-human hepatocellular carcinoma effects of tumor necrosis factor-related apoptosis-inducing ligand in vitro & in vivo.

AIM: To investigate the effect of over-expression of Bcl-2 protein on Trail protein-induced apoptosis in human hepatoma cells, and the cytotoxicity of Trail protein on human hepatoma cells in vitro and in vivo. METHODS: The Trail gene was cloned and expressed in E coli. The cytotoxicity of the recombinant Trail protein was assayed on human hepatoma cells in vitro and in vivo. The cell viability was assessed by trypan blue exclusion. The stable human hepatoma cells clone in which Bcl-2 protein over-expressed was established by transfecting eukaryotic expression plasmid pcDNA3-Bcl-2 into BEL-7404 human hepatoma cells, and was selected with G418 400 mg/L. RESULTS: The recombinant Trail protein actively killed human hepatoma cells tested in this study such as BEL-7404, BEL-7402, and SMMC-7721. Over-expression of Bcl-2 protein could inhibit apoptosis induced by Trail in BEL-7404 human hepatoma cells in vitro. It was obvious that the purified recombinant Trail protein could inhibit tumor formation of BEL-7404 human hepatoma cells in nude mice. CONCLUSION: The recombinant Trail protein could kill human hepatoma cells in vitro and in vivo. Over-expression of Bcl-2 protein could inhibit Trail-induced apoptosis in BEL-7404 human hepatoma cells. The results suggested that Trail might be a potential agent for the liver cancer therapy.

Bcl-2 over-expression and activation of protein kinase C suppress the trail-induced apoptosis in Jurkat T cells.

Trail, a tumor necrosis factor-related apoptosis-inducing ligand, is a novel potent endogenous activator of the cell death pathway through the activation of cell surface death receptors Trail-R1 and Trail-R2. Its role, like FasL in activation-induced cell death (AICD), has been demonstrated in immune system. However the mechanism of Trail induced apoptosis remains unclear. In this report, the recombinant Trail protein was expressed and purified. The apoptosis-inducing activity and the regulation mechanism of recombinant Trail on Jurkat T cells were explored in vitro. Trypan blue exclusion assay demonstrated that the recombinant Trail protein actively killed Jurkat T cells in a dose-dependent manner. Trail-induced apoptosis in Jurkat T cells were remarkably reduced by Bcl-2 over expression in Bcl-2 gene transfected cells. Treatment with PMA (phorbol 12-myristate 13-acetate), a PKC activator, suppressed Trail-induced apoptosis in Jurkat T cells. The inhibition of apoptosis by PMA was abolished by pretreatment with Bis, a PKC inhibitor. Taken together, it was suggested that Bcl-2 over-expression and PMA activated PKC actively down-regulated the Trail-mediated apoptosis in Jurkat T cell.

B cell lines from a subset of patients with common variable immunodeficiency undergo enhanced apoptosis associated with an increased display of CD95 (Apo-1/fas), diminished CD38 expression, and decreased IgG and IgA production.

Investigation of common variable immunodeficiency (CVI) is hampered by lack of a suitable in vitro models. We have developed EBV-transformed B lymphoblastoid cell lines from a selected subset of CVI patients and characterized them for phenotypic and functional properties that provide evidence for their representation of the CVI disease state. B cell lines from the patients expressed increased levels of sIgM and reduced levels of sIgD and sIgG. Essentially none of the CVI-derived B cell lines produced IgG and IgA while all produced IgM, in contrast to normal B cell lines that produced large amounts of IgG and IgM and detectable levels of IgA. Expression of CD95 (fas/Apo-1), a molecule that can induce apoptosis, was increased on the CVI B cell lines while CD38, a novel signaling molecule whose stimulation may prevent apoptosis, showed reduced expression. The B cell lines from the CVI patients exhibit increased apoptosis in vitro spontaneously, in response to anti-CD95 mAb and to X-irradiation. These phenotypic and functional changes are similar to findings on freshly derived B cells from the patients. EBV-derived B cell lines from patients with hyper-IgM immunodeficiency and X-linked agammaglobulinemia did not demonstrate increased CD95 expression or enhanced apoptosis. Thus the EBV-derived B cell lines from our selected CVI patients manifest many characteristics of the patients' fresh cells and may provide critical reagents for the further elucidation of the nature of the B cell dysfunction in the selected subset of CVI patients.

B cells from a distinct subset of patients with common variable immunodeficiency (CVID) have increased CD95 (Apo-1/fas), diminished CD38 expression, and undergo enhanced apoptosis.

We investigated the role of apoptosis in the differentiation failure of B cells from a selected subpopulation of patients with CVID delineated by B cell surface marker analysis, in vitro IgE response, and molecular markers of B cell VH gene repertoire. These patients had altered display of B cell surface molecules that play a role in apoptosis. The patients' B cells had a 4.5-250-fold increase in CD95 (Apo-1, fas) expression and increased CD95 display on their T cells. CD38, a molecule important in preventing germinal centre B cell apoptosis, was reduced on the patients' B cells. The expression of this molecule was inducible on the CVID lymphocytes with retinoic acid. Increased spontaneous apoptosis in vitro was observed with the patients' B (23%) and T cells (10%) compared with normal cells (13% and 3%, respectively). Stimulation in vitro with IL-4 and CD40 rescued the B cells from apoptosis and allowed for their differentiation. However, IL-4 plus alpha CD40-driven immunoglobulin production was not quantitatively or qualitatively normal. Failure to overcome apoptosis, a normal step in germinal centre B cell development, may be involved in the lack of differentiation seen in this subset of CVID patients.

Metallo-Carbohedrenes [M8C12+ (M = V, Zr, Hf, and Ti)]: A Class of Stable Molecular Cluster Ions.

Findings of magic peaks corresponding to M(8)C(12)(+) (M = V, Zr, and Hf) formed from reactions of the respective metals with various small hydrocarbons, in conjunction with recent findings for the titanium system, establish metallo-carbohedrenes as a stable general class of molecular cluster ions. A dodecahedral structure of T(h) point symmetry accounts for the stability of these ionic clusters.

Ti8C12+-Metallo-Carbohedrenes: A New Class of Molecular Clusters?

During the course of studying the dehydrogenation reactions of hydrocarbons by titanium atoms, ions, and clusters, an exceptionally stable and abundant cluster which contains 8 titaniums and 12 carbons was discovered. "Titration" reactions with ND(3) reveal the uptake of eight molecules, pointing to the fact that the titanium atoms are at exposed positions of similar coordination. A dodecahedral structure of T(h) point group symmetry is proposed to account for the unusual stability of this molecular cluster. The Ti(8)C(12)(+) dodecahedron has 12 pentagonal rings and each of the rings is formed by two titanium and three carbon atoms, where each titanium is bound to three carbons. Based on the model, it is expected that neutral Ti(8)C(12) would be a stable metallo-carbododecahedral molecule and may comprise one member of a new class of molecules, namely metallo-carbohedrenes.

Evidence for the polymerization of ethylene catalyzed by ti(+) in the gas phase.

In this communication, we report the polymerization of ethylene molecules induced by an atomic ion, namely Ti(+), in the gas phase. The experiments are performed by using a newly built selected ion drift tube with laser vaporization source apparatus operated at thermal energies. 50 far, up to twenty ethylene molecules are found to react with Ti(+), The evidence that a large number of ethylene molecules react with, and become bonded onto, Ti(+) at room temperature strongly suggests that Ti(+) induces a reaction between the ethylene molecules that leads to the formation of an ethylene polymer.

Establishment of a human B cell line that responds specifically to B cell growth factor.

A human B cell line (3D5) that responds specifically to B cell growth factor (BCGF) has been developed by a sequence of Staphylococcus aureus Cowen I activation, EB virus immortalization, and cloning. Proliferative response to PHA-stimulated T cell supernatant (PHA-T-Sup) and nonresponsiveness to rIL-2 stimulation were factors used to screen positive cells. Phenotype analysis with a flow cytometer indicated that: 1) 3D5 is a B cell line: 100% of the cells were positive for B1 marker and 59% were positive for sIg, while T3 and Mo 1 were negative; 2) 3D5 is an activated B cell line: both Tac and 4F2 markers of activated (but not of resting) B cells were 100% positive; 3) 3D5 expresses high molecular weight BCGF (HMW-BCGF) receptor-associated epitope BA5. 3D5 cells proliferated in response to cpBCGF stimulation in a dose-dependent manner. HMW-BCGF also induced 3D5 cells to proliferate. Interestingly, no proliferation could be detected in the presence of rIL-2, rIL-4, or rIFN-r. The data show that 3D5 cells are specifically BCGF-responsive B cells. Using 3D5 cells as target, BCGF activity was detected in crude BCGF preparation sedimented by 85% (NH4)2SO4 and chromatographed in a DEAE-Sephadex A-25 column from PHA-T-Sup. T24 cell supernatant with B cell differentiation factor (BCDF) activity could not induce 3D5 cells to differentiate into immunoglobulin-secreting cells.