Theoretical study on the molecular mechanism for the reaction of VO2+ with C2H4

The complex reaction between VO2+ ((1)A(1)/(3)A) and C2H4 (Ag-1(g)/(3)A(1)) to yield VO+ ((1)Delta/(3)Sigma) and CH3CHO ('A'/(3)A) has been studied by means of B3LYP/6-31G* and B3LYP/6-311G(2d,p) calculations. The structures of all reactants, products, intermediates, and transition structures of this reaction have been optimized and characterized at the fundamental singlet and first excited triplet electronic states. Crossing points are localized, and possible spin inversion processes are discussed by means of the intrinsic reaction coordinate approach. Relevant stationary points along the most favorable reaction pathways have been studied at the CCSD/6-311G(2d,p)//B3LYP/6-311G(2d,p) calculation level. The theoretical results allow the development of thermodynamic and kinetic arguments about the reaction pathways of the title process. In the singlet state, the first step is the barrierless obtention of a reactant complex associated with the formation of a V-C bond, while in the triplet state a three-membered ring addition complex with the V bonded to the two C atoms is obtained. Similar behavior is found in the exit channels: the product complexes can be formed from isolated products without barriers. The reactant and product complexes are the most stable stationary points in the singlet and triplet electronic states. From the singlet state reactant complex, two reaction pathways are posssible to reach the triplet state product complex. (i) A mechanism in which a hydrogen transfer process is the first and rate limiting step and the second step is an oxygen transfer between vanadium and carbon atoms with a concomitant change in the spin state. The crossing point between singlet and triplet spin states is not kinetically relevant because it takes place at a later stage occurring in the exit channel. (ii) A mechanism in which the first stage renders a four-membered ring between vanadyl cation and the ethylene fragment and an oxygencarbon bond is formed; on going from this minimum to the second transition structure, associated with a carbon-vanadium bond breaking process, the crossing point between singlet and triplet spin states is reached. The final step is the hydrogen transfer between both carbon atoms to yield the product complex. In this case the spin change opens a lower barrier pathway. The transition structures with larger values of relative energies for both reactive channels of VO2+ ((1)A(1)) + C2H4 (Ag-1) --> VO+ ((3)Sigma) + CH3CHO ((1)A') present similar energies, and the two reaction pathways can be considered as competitive.

On the dynamic behaviour of the "click" mechanism in dipteran flight

In this paper, the dynamic behaviour of the "click" mechanism is analysed. A more accurate model is used than in the past, in which the limits of movement due to the geometry of the flight mechanism are imposed. Moreover, the effects of different damping models are investigated. In previous work, the damping model was assumed to be of the linear viscous type for simplicity, but it is likely that the damping due to drag forces is nonlinear. Accordingly, a model of damping in which the damping force is proportional to the square of the velocity is used, and the results are compared with the simpler model of linear viscous damping. Because of the complexity of the model an analytical approach is not possible so the problem has been cast in terms of non-dimensional variables and solved numerically. The peak kinetic energy of the wing root per energy input in one cycle is chosen to study the effectiveness of the "click" mechanism compared with a linear resonant mechanism. It is shown that, the "click" mechanism has distinct advantages when it is driven below its resonant frequency. When the damping is quadratic, there are some further advantages compared to when the damping is linear and viscous, provided that the amplitude of the excitation force is large enough to avoid the erratic behaviour of the mechanism that occurs for small forces. (C) 2011 Elsevier Ltd. All rights reserved.

Vibration Attenuation in Rotating Machines Using Smart Spring Mechanism

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of PbS impurity on crystallization mechanism of phosphate glasses studied by differential scanning calorimetry

In this work, differential scanning calorimetry (DSC) was used to study effect of PbS impurity on crystallization mechanism of phosphate glasses. Bulk glasses presented one crystallization peak while powdered glasses presented two distinct crystallization peaks. For both undoped and doped glasses were determined the activation energies for the crystallization and the Avrami n parameters. The activation energies for undoped phosphate glass were 336 +/- 6 and 213 +/- 3 kJ mol(-1), respectively, associated with first and second crystallization peaks. For doped glass, the obtained energies were 373 +/- 9 and 286 +/- 7 kJ mol(-1). The calculated Avrami parameters, based on first crystallization peaks, for undoped and doped glasses were 2.25 +/- 0.01 and 1.75 +/- 0.02, respectively. These values suggest that the first DSC peak, in both glasses, may be associated with surface crystallization. (C) 2002 Elsevier B.V. B.V. All rights reserved.

Sulcus vocalis: evidence for autosomal dominant inheritance

We found evidence of autosomal dominant hereditary transmission of sulcus vocalis. Four dysphonic patients from three generations of the same family were submitted to videolaryngoscopic examination (three patients) and to direct laryngoscopy ( one patient) to diagnose the hoarseness. Sulcus vocalis was diagnosed in all four patients. The finding of four affected individuals in three generations, with vertical transmission affecting man and women, is more consistent with autosomal dominant inheritance pattern; it is an etiological model that we propose for the sulcus vocalis in this pedigree.

Managing the dominant follicle in lactating dairy cows

Reproductive efficiency is not optimal in high-producing dairy cows. Although many aspects of ovarian follicular growth in cows are similar to those observed in heifers, there are numerous specific differences in follicular development that may be linked with changes in reproductive physiology in high-producing lactating dairy cows. These include: I) reduced circulating estradiol (E2) concentrations near estrus, 2) ovulation of follicles that are larger than the optimal size, 3) increased double ovulation and twinning, and 4) increased incidence of anovulation with a distinctive pattern of follicle growth in anovular dairy cows. The first three changes become more dramatic as milk production increases, although anovulation has not generally been associated with level of milk production. To overcome reproductive inefficiencies in dairy cows, reproductive management programs have been developed to synchronize ovulation and enable the use of timed AI in lactating dairy cows. Effective regulation of the CL, follicles, and hormonal environment during each part of the protocol is critical for optimizing these programs. This review discusses the distinct aspects of follicular development in lactating dairy cows and the methodologies that have been utilized in the past two decades in order to manage the dominant follicle during synchronization of ovulation and timed AI programs. (C) 2011 Published by Elsevier B.V.

Mechanism of calcium hydroxide-induced neutrophil migration into air-pouch cavity

The aim of this study was to investigate cellular migration induced by calcium hydroxide to air-pouch cavities in mice. The migration was more specific to neutrophil and was dose and time dependent (peaking 96 h after stimulation). This migration was inhibited by pretreatment with thalidomide, indomethacin, MK886, meloxicam, dexamethasone, MK886 associated with indomethacin, and MK886 associated with indomethacin and dexamethasone. The air-pouch exudate from animals stimulated with calcium hydroxide showed an increase of leukotriene-B4 (LTB4), interleukin-1 beta, tumor necrosis factor alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) release. Pretreatment with 3% thioglycollate increased the macrophage population in the air pouch but did not change neutrophil migration. Depleting the resident mast cells through chronic pretreatment with compound 48/80 did not alter neutrophil migration in response to calcium hydroxide. It was possible to conclude that calcium hydroxide-induced neutrophil migration to the air-pouch cavity in mice is mediated by LTB4, TNF-alpha, KC, MIP-2, and prostaglandins, but it was not dependent on macrophages or mast cells.

A dominant function of p38 mitogen-activated protein kinase signaling in receptor activator of nuclear factor-kappa B ligand expression and osteoclastogenesis induction by Aggregatibacter actinomycetemcomitans and Escherichia coli lipopolysaccharide

Background and Objective: Lipopolysaccharide from gram-negative bacteria is one of the microbial-associated molecular patterns that initiate the immune/inflammatory response, leading to the tissue destruction observed in periodontitis. The aim of this study was to evaluate the role of the p38 mitogen-activated protein kinase (MAPK) signaling pathway in lipopolysaccharide-induced receptor activator of nuclear factor-kappa B ligand (RANKL) expression by murine periodontal ligament cells.Material and Methods: Expression of RANKL and osteoprotegerin mRNA was studied by reverse transcription-polymerase chain reaction upon stimulation with lipopolysaccharide from Escherichia coli and Aggregatibacter actinomycetemcomitans. The biochemical inhibitor SB203580 was used to evaluate the contribution of the p38 MAPK signaling pathway to lipopolysaccharide-induced RANKL and osteoprotegerin expression. Stable cell lines expressing dominant-negative forms of MAPK kinase (MKK)-3 and MKK6 were generated to confirm the role of the p38 MAPK pathway. An osteoclastogenesis assay using a coculture model of the murine monocytic cell line RAW 264.7 was used to determine if osteoclast differentiation induced by lipopolysaccharide-stimulated periodontal ligament was correlated with RANKL expression.Results: Inhibiting p38 MAPK prior to lipopolysaccharide stimulation resulted in a significant decrease of RANKL mRNA expression. Osteoprotegerin mRNA expression was not affected by lipopolysaccharide or p38 MAPK. Lipopolysaccharide-stimulated periodontal ligament cells increased osteoclast differentiation, an effect that was completely blocked by osteoprotegerin and significantly decreased by inhibition of MKK3 and MKK6, upstream activators of p38 MAPK. Conditioned medium from murine periodontal ligament cultures did not increase osteoclast differentiation, indicating that periodontal ligament cells produced membrane-bound RANKL.Conclusion: Lipopolysaccharide resulted in a significant increase of RANKL in periodontal ligament cells. The p38 MAPK pathway is required for lipopolysaccharide-induced membrane-bound RANKL expression in these cells.

Loss of Expression and Function of SOCS3 Is an Early Event in HNSCC: Altered Subcellular Localization as a Possible Mechanism Involved in Proliferation, Migration and Invasion

Background: Suppressor of cytokine signaling 3 (SOCS3) is an inducible endogenous negative regulator of signal transduction and activator of transcription 3 (STAT3). Epigenetic silencing of SOCS3 has been shown in head and neck squamous cell carcinoma (HNSCC), which is associated with increased activation of STAT3. There is scarce information on the functional role of the reduction of SOCS3 expression and no information on altered subcellular localization of SOCS3 in HNSCC.Methodology/Principal Findings: We assessed endogenous SOCS3 expression in different HNSCC cell lines by RT-qPCR and western blot. Immunofluorescence and western blot were used to study the subcellular localization of endogenous SOCS3 induced by IL-6. Overexpression of SOCS3 by CMV-driven plasmids and siRNA-mediated inhibition of endogenous SOCS3 were used to verify the role of SOCS3 on tumor cell proliferation, viability, invasion and migration in vitro. In vivo relevance of SOCS3 expression in HNSCC was studied by quantitative immunohistochemistry of commercially-available tissue microarrays. Endogenous expression of SOCS3 was heterogeneous in four HNSCC cell lines and surprisingly preserved in most of these cell lines. Subcellular localization of endogenous SOCS3 in the HNSCC cell lines was predominantly nuclear as opposed to cytoplasmic in non-neoplasic epithelial cells. Overexpression of SOCS3 produced a relative increase of the protein in the cytoplasmic compartment and significantly inhibited proliferation, migration and invasion, whereas inhibition of endogenous nuclear SOCS3 did not affect these events. Analysis of tissue microarrays indicated that loss of SOCS3 is an early event in HNSCC and was correlated with tumor size and histological grade of dysplasia, but a considerable proportion of cases presented detectable expression of SOCS3.Conclusion: Our data support a role for SOCS3 as a tumor suppressor gene in HNSCC with relevance on proliferation and invasion processes and suggests that abnormal subcellular localization impairs SOCS3 function in HNSCC cells.

Serotonergic mechanism of the lateral parabrachial nucleus and relaxin-induced sodium intake

It has been shown that central or peripheral injections of the peptide relaxin induces water intake, not sodium intake in rats. Important inhibitory mechanisms involving serotonin and other neurotransmitters in the control of water and NaCl intake have been demonstrated in the lateral parabrachial nucleus (LPBN). In the present Study, we investigated the effects of bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN on intracerebroventricular (i.c.v.) relaxin-induced water and NaCl intake in rats. Additionally, the effect of the blockade of central angiotensin AT(1) receptors with i.c.v. losartan on relaxin-induced water and NaCl intake in rats treated with methysergide into the LPBN was also investigated. Male Holtzman rats with cannulas implanted into the lateral ventricle (LV) and bilaterally in the LPBN were used. Intracerebroventricular injections of relaxin (500 ng/l mul) induced water intake (5.1+/-0.7 ml/120 min), but not significant 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Bilateral injections of methysergide (4 mug/0.2 mul) into the LPBN strongly stimulated relaxin-induced 1.8% NaCl intake (34.5+/-10.9 ml/120 min) and slightly increased water intake (10.5+/-4.9 ml/120 min). The pretreatment with i.c.v. losartan (100 mug/l mul) abolished the effects of i.c.v. relaxin combined with LPBN methysergide on 1.8% NaCI intake (0.5+/-0.4 ml/120 min). Losartan (100 mug/l mul) also abolished relaxin-induced water intake in rats injected with methysergide into the LPBN (1.6+/-0.8 ml/120 min) or not (0.5+/-0.3 ml/120 min). Losartan (50 mug/l mul) partially reduced the effects of relaxin. The results show that central relaxin interacting with central angiotensinergic mechanisms induces NaCl intake after the blockade of LPBN serotonergic mechanisms. (C) 2004 Elsevier B.V. All rights reserved.