Antigenic Activity of Bacterial Endodontic Contents from Primary Root Canal Infection with Periapical Lesions against Macrophage in the Release of Interleukin-1 beta and Tumor Necrosis Factor alpha

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

NEUTRINOLESS DOUBLE-BETA DECAY IN AN SU(3)(L)CIRCLE-TIMES-U(1)(N) MODEL

We consider a model for the electroweak interactions with the SU(3)(L) circle times U(1)(N) gauge symmetry. We show that the conservation of the quantum number F = L+B forbids the appearance of massive neutrinos and the neutrinoless double-beta decay (beta beta)(0 nu). Explicit or/and spontaneous breaking of F implies that the neutrinos have an arbitrary mass. In addition the (beta beta)(0 nu) decay also has some channels that do not depend explicitly on the neutrino mass.

Low protein diet confers resistance to the inhibitory effects of interleukin1 beta on insulin secretion in pancreatic islets

High protein content in the diet during childhood and adolescence has been associated to the onset insulin-dependent diabetes mellitus. We investigated the effect of interleukin-1 beta (IL-I beta) on insulin secretion, glucose metabolism, and nitrite formation by islets isolated from rats fed with normal protein (NP, 17%) or low protein (LP, 6%) after weaning. Pretreatment of islets with IL-1 beta for 1 h or 34 h inhibited the insulin secretion induced by glucose in both groups, but it was less marked in LP than in NP group. Islets from LP rats exhibited a decreased IL-1 beta -induced nitric oxide (NO) production, lower inhibition of D-[(UC)-C-14]-glucose oxidation to (CO2)-C-14, and less pronounced effect of IL-1 beta on alpha -ketoisocaproic acid-induced insulin secretion than NP islets. However, when the islets were stimulated by high concentrations of K+ the inhibitory effect of IL-1 beta on insulin secretion was not different between groups. In conclusion, protein restriction protects beta -cells of the deleterious effect of IL-1 beta, apparently, by decreasing NO production. The lower NO generation in islets from protein deprived rats may be due to increased free fatty acids oxidation and consequent alteration in Ca2+ homeostasis. (C) 2001 Elsevier B.V. All rights reserved.

Thermal behavior of Cu-Al alloys near the alpha-Cu-Al solubility limit

The thermal behavior of Cu-Al alloys with 17, 19 and 21 at.%Al was examined by differential thermal analysis (DTA), differential scanning calorimetry (DSC), X-ray diffractometry (XRD), optical microscopy (OM) and scanning electron microscopy (SEM). The presence of the gamma phase (Al4Cu9) was clearly detected for the Cu-19 at.%Al alloy and caused the alpha (2) phase disordering process in two stages. The tendency to increase the alpha (2) dissolution precipitates with the increase in the Al content seems to be reverted for compositions at about 21 at.%Al and the heating/cooling ratio seems to influence the thermal response of this process. The presence of the endothermic peak corresponding to the beta (1)--> beta transformation depends on an incomplete beta decomposition reaction. The variation of the heating rate showed that the beta (1)-->(alpha+gamma (1)) decomposition is the dominant reaction for alloys containing 19 and 21 at.%Al.

Effect of thermal pasteurization and concentration on carotenoid composition of Brazilian Valencia orange juice

Changes in carotenoid pigment content of Brazilian Valencia orange juices due to thermal pasteurization and concentration were studied. Total carotenoid pigment content loss was not significant after thermal pasteurization and concentration. However, thermal effects on carotenoid pigment contents, especially violaxanthin and lutein, were clearly observed and significant (P < 0.05). Pasteurization reduced the content of violaxanthin by 38% and lutein by 20%. The concentration process resulted in loss of lutein (17%). With the loss of lutein, beta-cryptoxanthin became the major carotenoid in the pasteurized and concentrated juices. The provitarnin A content of the juice (beta-carotene, alpha-carotene and beta-cryptoxanthin) and the amount of zeaxanthin, which are considered to be active against age-related macular degeneration and cataracts, did not significantly decrease after pasteurization and concentration. (c) 2006 Elsevier Ltd. All rights reserved.

Major carotenoid composition of Brazilian Valencia orange juice: Identification and quantification by HPLC

The carotenoid composition of Brazilian Valencia orange juice was determined by open column chromatography (OCC) and high-performance liquid chromatography. Carotenoid pigments were extracted using acetone and saponified using 10% methanolic potassium hydroxide. Sixteen pigments were isolated by OCC and identified as alpha-carotene, zeta-carotene, beta-carotene, alpha-cryptoxanthin, beta-cryptoxanthin, lutein-5,6-epoxide, violaxanthin, lutein, antheraxanthin, zeaxanthin, luteoxanthin A, luteoxanthin B, mutatoxanthin A, mutatoxanthin B, auroxanthin B and trollichrome B. Thirteen carotenoid pigments were separated using a ternary gradient (acetonitrile-methanol-ethyl acetate) elution on a C-18 reversed-phase column. Among these, violaxanthin, lutein, zeaxanthin, beta-cryptoxanthin, zeta-carotene, alpha-carotene, and beta-carotene were quantified. The total carotenoid content was 12 +/- 6.7 mg/1, and the major carotenoids were lutein (23%), beta-cryptoxanthin (21%), and zeaxanthin (20%). 2005 Elsevier Ltd. All rights reserved.

Protective effects of Tacrolimus, a calcineurin inhibitor, in experimental periodontitis in rats

Objective: Periodontitis is a well-appreciated example of leukocyte-mediated bone loss and inflammation with pathogenic features similar to those observed in other inflammatory diseases, such as arthritis. Since Tacrolimus, is an immunomodulatory drug used for the treatment of some cases of arthritis, we hypothesized that it may modulate periodontal disease.Design: Using a murine model of ligature-induced periodontal disease, we assessed the effects of daily administrations of Tacrolimus (1 mg/kg body weight) on bone loss, enzymatic (myeloperoxidase) analysis, differential white blood cells counts, airpouch exudate and cytokine expression for 5-30 days.Results: Radiographic, enzymatic (myeloperoxidase) and histological analysis revealed that Tacrolimus reduced the severity of periodontitis. More specifically, Tacrolimus suppressed the expression of serum interleukin (IL-1 beta), tumour necrosis factor (TNF-alpha), IL-6, airpouch exudate PGE(2) and leukocytosis usually observed after the induction of periodontitis. Tacrolimus treatment in periodontitis-induced rats conferred protection against the inflammation-induced tissue and bone loss associated with periodontitis, through a mechanism involving IL-1 beta, TNF-alpha and IL-6.Conclusions: the effects of Tacrolimus on periodontal disease pathogenesis may provide clues to a novel approach to host modulation therapy in destructive periodontal disease. (C) 2007 Elsevier Ltd. All rights reserved.

The Potential of p38 MAPK Inhibitors to Modulate Periodontal Infections

Periodontal disease initiation and progression occurs as a consequence of the host immune inflammatory response to oral pathogens. The innate and acquired immune systems are critical for the proper immune response. LPS, an outer membrane constituent of periodontal pathogenic bacteria, stimulates the production of inflammatory cytokines IL-1 beta TNF alpha IL-6 and RANKL either directly or indirectly. In LPS-stimulated cells, the induction of cytokine expression requires activation of several signaling pathways including the p38 MAPK pathway. This review will discuss the significance of the p38 MAPK pathway in periodontal disease progression and the potential therapeutic consequences of pharmacological antagonism of this pathway in the treatment of periodontal diseases.

Correlation between Clinical/Radiographic Features and Inflammatory Cytokine Networks Produced by Macrophages Stimulated with Endodontic Content

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Periacinar Retraction Clefting in Nonneoplastic and Neoplastic Prostatic Glands: Artifact or Molecular Involvement

A space between neoplastic acini and prostatic stroma is not rare and studies have interpreted this as an artifact, considering the absence of endothelial cells indicating vascular invasion. Thus, the aims of this work were to characterize and correlate the occurrence and extent of retraction clefting with the reactivities of alpha and beta dystroglycan (alpha DG, beta DG), laminin, matrix metalloproteinase 2 (MMP-2), p63, insulin-like growth factor 1(IGF-1), vimentin, and fibroblast growth factor 2 (FGF-2). The study was based on nonneoplastic and neoplastic prostatic tissues obtained from necropsies and retropubic radical prostatectomies. The results showed that periacinar retraction clefting was significantly more frequent in prostatic carcinoma samples than in normal prostatic acini. Most of the neoplastic acini (72.0%) showed retraction clefting of more than 50% of circumference, which were significantly more frequent in Gleason score 7 and 6. Decreased collagen and reticular and elastic fibers were verified in the stroma around neoplastic acini. Weak and discontinuous alpha DG, beta DG, and laminin immunoreactivities and intensified MMP-2, vimentin, IGF-1 and FGF-2 immunoreactivities were verified in the neoplastic acini; p63 immunoreactivity was negative in all carcinomas. Thus, these findings showed that the lack of epithelial basal cells, DGs, and laminin and increased MMP-2, IGF-1, and FGF-7 could be considered important pathways in periacinar retraction occurrence. This study demonstrated the origin of and the biological mechanisms responsible for periacinar retraction clefting in prostatic carcinoma.

Fibrosis-related gene expression in the prostate is modulated by doxazosin treatment

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Production of xylanolytic enzymes by Penicillium janczewskii

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Zeros of Jacobi functions of second kind

The number of zeros in (- 1, 1) of the Jacobi function of second kind Q(n)((alpha, beta)) (x), alpha, beta > - 1, i.e. The second solution of the differential equation(1 - x(2))y (x) + (beta - alpha - (alpha + beta + 2)x)y' (x) + n(n + alpha + beta + 1)y(x) = 0,is determined for every n is an element of N and for all values of the parameters alpha > - 1 and beta > - 1. It turns out that this number depends essentially on alpha and beta as well as on the specific normalization of the function Q(n)((alpha, beta)) (x). Interlacing properties of the zeros are also obtained. As a consequence of the main result, we determine the number of zeros of Laguerre's and Hermite's functions of second kind. (c) 2005 Elsevier B.V. All rights reserved.

Monotonicity of zeros of Jacobi polynomials

Denote by x(nk)(alpha, beta), k = 1...., n, the zeros of the Jacobi polynornial P-n((alpha,beta)) (x). It is well known that x(nk)(alpha, beta) are increasing functions of beta and decreasing functions of alpha. In this paper we investigate the question of how fast the functions 1 - x(nk)(alpha, beta) decrease as beta increases. We prove that the products t(nk)(alpha, beta) := f(n)(alpha, beta) (1 - x(nk)(alpha, beta), where f(n)(alpha, beta) = 2n(2) + 2n(alpha + beta + 1) + (alpha + 1)(beta + 1) are already increasing functions of beta and that, for any fixed alpha > - 1, f(n)(alpha, beta) is the asymptotically extremal, with respect to n, function of beta that forces the products t(nk)(alpha, beta) to increase. (c) 2007 Elsevier B.V. All rights reserved.

On the behaviour of zeros of Jacobi polynomials

Denote by x(n,k)(alpha, beta) and x(n,k) (lambda) = x(n,k) (lambda - 1/2, lambda - 1/2) the zeros, in decreasing order, of the Jacobi polynomial P-n((alpha, beta))(x) and of the ultraspherical (Gegenbauer) polynomial C-n(lambda)(x), respectively. The monotonicity of x(n,k)(alpha, beta) as functions of a and beta, alpha, beta > - 1, is investigated. Necessary conditions such that the zeros of P-n((a, b)) (x) are smaller (greater) than the zeros of P-n((alpha, beta))(x) are provided. A. Markov proved that x(n,k) (a, b) < x(n,k)(&alpha;, &beta;) (x(n,k)(a, b) > x(n,k)(alpha, beta)) for every n is an element of N and each k, 1 less than or equal to k less than or equal to n if a > alpha and b < &beta; (a < alpha and b > beta). We prove the converse statement of Markov's theorem. The question of how large the function could be such that the products f(n)(lambda) x(n,k)(lambda), k = 1,..., [n/2] are increasing functions of lambda, for lambda > - 1/2, is also discussed. Elbert and Siafarikas proved that f(n)(lambda) = (lambda + (2n(2) + 1)/ (4n + 2))(1/2) obeys this property. We establish the sharpness of their result. (C) 2002 Elsevier B.V. (USA).