Hasil untuk "Pathology"

Erik K. Alexander, Giulia C. Kennedy, Z. Baloch et al.

Stanley R Hamilton, L. Aaltonen

N. Haboubi

N. Rothwell, G. Luheshi

P. Rosen

W. Travis

V. Yajnik

Antonio Sergio Altieri de Moraes Pitombo

O artigo trata da questão da decretação de prisão cautelar como instrumento de agentes da Justiça Criminal  para influir na autodeterminação do preso quanto à ampla defesa, constrangendo-o a barganhar direitos, por meio de colaboração processual. Discute-se se a teoria do dilema do prisioneiro não se exibe uma forma de tortura psicológica, sob a perspectiva dos tratados internacionais.

Karolina Banyś, Małgorzata Jelińska, Małgorzata Wrzosek et al.

The purpose of this study was to evaluate the effect of genistein in nano, micro, and macro forms on the intensity of the DMBA-induced tumor process in rats and to understand the mechanisms of this action. The effect of genistein supplementation on the content of selected eicosanoids (HETEs, HODE, and HEPE) in the serum of rats was evaluated. The levels and expression of genes encoding various pro-inflammatory cytokines (IL-1, IL-6) and MMP-9 in the blood of rats were also investigated. The biological material for the study was blood obtained from female rats of the Sprague Dawley strain (n = 32). The animals were randomly divided into four groups: animals without supplementation, and animals supplemented at a dose of 0.2 mg/kg b.w. (0.1 mg/mL) with macro, micro (587 ± 83 nm), or nano (92 ± 41 nm) genistein. To induce mammary neoplasia (adenocarcinoma), rats were given 7,12-dimethyl-1,2-benz[a]anthracene (DMBA). The content of selected eicosanoids was determined by liquid chromatography with UV detection. An immunoenzymatic method was used to determine the content of cytokines and MMP-9. The expression of the <i>IL-6, IL-1beta,</i> and <i>MMP-9</i> genes was determined with quantitative real-time PCR (qRT-PCR) using TaqMan probes. Based on the study, it was shown that supplementation of animals with genistein in macro, micro, and nano forms increased the intensity of the tumor process in rats. It was shown that the content of 12-HEPE, HODE, and 12-HETE in the serum of genistein-supplemented rats was statistically significantly lower with respect to the content of the aforementioned markers in the serum of rats receiving only a standard diet, devoid of supplementation. It was found that animals supplemented with nano-, micro-, and macrogenistein had higher levels of metalloproteinase-9, MMP-9, compared to animals without supplementation. There was a significant increase in MMP-9 gene expression in the blood of macrogenistein-supplemented animals, relative to the other groups of rats. On the basis of the study, it was shown that supplementation of animals with nano-, micro-, and macrogenistein had an effect on the development of the tumor process. Dietary supplementation with genistein significantly decreased the level of selected eicosanoids, which may have significant impacts on cancer development and progression.

S. Jacques, J. Ramella-Roman, Kenneth Lee

Jiang Gu, C. Korteweg

Severe acute respiratory syndrome (SARS) is an emerging infectious viral disease characterized by severe clinical manifestations of the lower respiratory tract. The pathogenesis of SARS is highly complex, with multiple factors leading to severe injury in the lungs and dissemination of the virus to several other organs. The SARS coronavirus targets the epithelial cells of the respiratory tract, resulting in diffuse alveolar damage. Several organs/cell types may be infected in the course of the illness, including mucosal cells of the intestines, tubular epithelial cells of the kidneys, neurons of the brain, and several types of immune cells, and certain organs may suffer from indirect injury. Extensive studies have provided a basic understanding of the pathogenesis of this disease. In this review we describe the most significant pathological features of SARS, explore the etiological factors causing these pathological changes, and discuss the major pathogenetic mechanisms. The latter include dysregulation of cytokines/chemokines, deficiencies in the innate immune response, direct infection of immune cells, direct viral cytopathic effects, down-regulation of lung protective angiotensin converting enzyme 2, autoimmunity, and genetic factors. It seems that both abnormal immune responses and injury to immune cells may be key factors in the pathogenesis of this new disease.

M. Pearson, R. Beever, B. Boine et al.

L. Barnes, R. Wilson, J. Bienias et al.

Sara Lofthag-Hansen, S. Huumonen, K. Gröndahl et al.

V. W. Yong

Zeynab Arbabi, Abdolali Banaiefar, Sajjad Arshadi et al.

Background and Aim: Metabolic syndrome refers to a set of metabolic disorders related to obesity, such as abdominal obesity, increased body fat mass, lipid disorders, hypertension, increased blood glucose, and insulin resistance. The present study was conducted with the aim of determining the effect of 8 weeks of CXWORX exercises combined with inulin consumption on some indicators of oxidative stress in obese women with metabolic syndrome. Materials and Methods: Forty eight obese women with metabolic syndrome in the age range of 30 to 40 years were randomly divided into Control, inulin, CX exercise and combined groups were included. Subjects were present in the laboratory environment and 5 cc of blood was taken from their brachial vein. Blood sample was taken to measure malondialdehyde and xanthine oxidase (pre-test). Then the aforementioned interventions were performed on the studied groups for a period of 8 weeks. Finally, blood sampling was done again to measure the variables (post-test). Results: The results of the correlated t-test revealed that in all three groups, the intervention led to a significant decrease in malondialdehyde compared to the pre-test; However, xanthine oxidase variable did not change significantly in the exercise group and significantly decreased in the inulin and combined groups compared to the pre-test. ANOVA results revealed that compared to the control group, the amount of malondialdehyde is significant only in the combined group (P≤0.05). The amount of this variable in the combined group decreased significantly compared to the exercise and inulin group (P≤0.05). No significant difference was observed between the exercise and inulin groups (P>0.05). Amount of xanthine oxidase, a significant difference had between the inulin and combination groups with the control group (P≤0.05). No significant difference was observed between the exercise and inulin groups (P>0.05). Despite this, a significant difference in xanthine oxidase levels was observed between the combined group with the exercise and inulin groups (P≤0.05). Conclusion: Based on the available findings, it is concluded that the implementation of CX exercises combined with the use of inulin reduces the oxidative stress function more than the application of each of them alone in women with metabolic syndrome.

Leonora Szabo, Amandine Grimm, Juan Antonio García-León et al.

Pathological abnormalities in the tau protein give rise to a variety of neurodegenerative diseases, conjointly termed tauopathies. Several tau mutations have been identified in the tau-encoding gene <i>MAPT</i>, affecting either the physical properties of tau or resulting in altered tau splicing. At early disease stages, mitochondrial dysfunction was highlighted with mutant tau compromising almost every aspect of mitochondrial function. Additionally, mitochondria have emerged as fundamental regulators of stem cell function. Here, we show that compared to the isogenic wild-type triple <i>MAPT</i>-mutant human-induced pluripotent stem cells, bearing the pathogenic N279K, P301L, and E10+16 mutations, exhibit deficits in mitochondrial bioenergetics and present altered parameters linked to the metabolic regulation of mitochondria. Moreover, we demonstrate that the triple tau mutations disturb the cellular redox homeostasis and modify the mitochondrial network morphology and distribution. This study provides the first characterization of disease-associated tau-mediated mitochondrial impairments in an advanced human cellular tau pathology model at early disease stages, ranging from mitochondrial bioenergetics to dynamics. Consequently, comprehending better the influence of dysfunctional mitochondria on the development and differentiation of stem cells and their contribution to disease progression may thus assist in the potential prevention and treatment of tau-related neurodegeneration.

P. LeBoit

L. Calderón-Garcidueñas, W. Reed, R. Maronpot et al.

D. Bennett, J. Schneider, J. Bienias et al.