Tissues In Normal Conditions Research Articles

CDNA Characterization and Expression of Selenium-Dependent CqGPx3 Isoforms in the Crayfish Cherax quadricarinatus under High Temperature and Hypoxia.

Glutathione peroxidase 3 (GPx3) is the only extracellular selenoprotein (Sel) that enzymatically reduces H2O2 to H2O and O2. Two GPx3 (CqGPx3) cDNAs were characterized from crayfish Cherax quadricarinatus. The nerve cord CqGPx3a isoform encodes for a preprotein containing an N-terminal signal peptide of 32 amino acid residues, with the mature Sel region of 192 residues and a dispensable phosphorylation domain of 36 residues. In contrast, the pereiopods CqGPx3b codes for a precursor protein with 19 residues in the N-terminal signal peptide, then the mature 184 amino acid residues protein and finally a Pro-rich peptide of 42 residues. CqGPx3 are expressed in cerebral ganglia, pereiopods and nerve cord. CqGPx3a is expressed mainly in cerebral ganglia, antennulae and nerve cord, while CqGPx3b was detected mainly in pereiopods. CqGPx3a expression increases with high temperature and hypoxia; meanwhile, CqGPx3b is not affected. We report the presence and differential expression of GPx3 isoforms in crustacean tissues in normal conditions and under stress for high temperature and hypoxia. The two isoforms are tissue specific and condition specific, which could indicate an important role of CqGPx3a in the central nervous system and CqGPx3b in exposed tissues, both involved in different responses to environmental stressors.

Diagnostic Value of HLA Typing in Pathogenesis of Cardiomyopathy.

Development of cardiomyopathy (CM) is dependent upon several factors. However, the reaction of the immune response against myocardial tissue due to microbial and viral infections plays an important role in this disease. Therefore, the purpose of this study is to investigate the relationship between HLAs and their pathogenic mechanisms in the incidence of CM. Relevant literature was identified by a PubMed search (1989-2017) of English-language papers using the terms "Cardiomyopathy", "Human leukocyte antigen or HLA", "immune response", and "polymorphism". If CM patients are afflicted with viral and microbial infections, HLA class II molecules, which are not expressed on myocardial tissue in normal conditions, are mainly expressed on it. As a result, these HLAs present self- antigens and provoke autoimmune responses against myocardial tissue. On the other hand, the occurrence of polymorphism as well as disrupted expression of miRNAs can affect HLA expression, leading to hypertrophy and fibrosis of cardiac muscle. Finally, it is inferred that the expression evaluation of HLAs as well as identification of polymorphisms in their coding genes can be effective diagnostic factors in the detection of people susceptible to CM.

Labeling galectin-3 for the assessment of myocardial infarction in rats.

BackgroundGalectin-3 is a ß-galactoside-binding lectin expressed in most of tissues in normal conditions and overexpressed in myocardium from early stages of heart failure (HF). It is an established biomarker associated with extracellular matrix (ECM) turnover during myocardial remodeling. The aim of this study is to test the ability of 123I-galectin-3 (IG3) to assess cardiac remodeling in a model of myocardial infarction (MI) using imaging techniques.MethodsRecombinant galectin-3 was labeled with iodine-123 and in vitro binding assays were conducted to test 123I-galectin-3 ability to bind to ECM targets. For in vivo studies, a rat model of induced-MI was used. Animals were subjected to magnetic resonance and micro-SPETC/micro-CT imaging two (2 W-MI) or four (4 W-MI) weeks after MI. Sham rats were used as controls. Pharmacokinetic, biodistribution, and histological studies were also performed after intravenous administration of IG3.ResultsIn vitro studies revealed that IG3 shows higher binding affinity (measured as counts per minute, cpm) (p < 0.05) to laminin (2.45 ± 1.67 cpm), fibronectin (4.72 ± 1.95 cpm), and collagen type I (1.88 ± 0.53 cpm) compared to bovine serum albumin (BSA) (0.88 ± 0.31 cpm). Myocardial quantitative IG3 uptake (%ID/g) was higher (p < 0.01) in the infarct of 2 W-MI rats (0.15 ± 0.04%) compared to control (0.05 ± 0.03%). IG3 infarct uptake correlates with the extent of scar (rs = 1, p = 0.017). Total collagen deposition in the infarct (percentage area) was higher (p < 0.0001) at 2 W-MI (24.2 ± 5.1%) and 4 W-MI (30.4 ± 7.5%) compared to control (1.9 ± 1.1%). However, thick collagen content in the infarct (square micrometer stained) was higher at 4 W-MI (20.5 ± 11.2 μm2) compared to control (4.7 ± 2.0 μm2, p < 0.001) and 2 W-MI (10.6 ± 5.1 μm2, p < 0.05).ConclusionsThis study shows, although preliminary, enough data to consider IG3 as a potential contrast agent for imaging of myocardial interstitial changes in rats after MI. Labeling strategies need to be sought to improve in vivo IG3 imaging, and if proven, galectin-3 might be used as an imaging tool for the assessment and treatment of MI patients.

Immunomodulatory properties of HLA-G in infectious diseases.

HLA-G is a nonclassical major histocompatibility complex molecule first described at the maternal-fetal interface, on extravillous cytotrophoblasts. Its expression is restricted to some tissues in normal conditions but increases strongly in pathological conditions. The expression of this molecule has been studied in detail in cancers and is now also beginning to be described in infectious diseases. The relevance of studies on HLA-G expression lies in the well known inhibitory effect of this molecule on all cell types involved in innate and adaptive immunity, favoring escape from immune control. In this review, we summarize the features of HLA-G expression by type of infections (i.e, bacterial, viral, or parasitic) detailing the state of knowledge for each pathogenic agent. The polymorphism, the interference of viral proteins with HLA-G intracellular trafficking, and various cytokines have been described to modulate HLA-G expression during infections. We also discuss the cellular source of HLA-G, according to the type of infection and the potential role of HLA-G. New therapeutic approaches based on synthetic HLA-G-derived proteins or antibodies are emerging in mouse models of cancer or transplantation, and these new therapeutic tools may eventually prove useful for the treatment of infectious diseases.

Measurements of the optical density of the alveolar process bone tissue of the jaws during periodontal diseases with the use of three-dimensional computed tomography

Aim. To determine the optical density of the alveolar process bone tissue in normal conditions and during various forms of periodontal pathology. Methods. With the use of clinical and radiographic methods examined were 120 patients (with a healthy periodontium, with chronic generalized catarrhal gingivitis of moderate severity, with chronic periodontitis of a mild, moderate and severe degree). On the three-dimensional computer tomograms in each group of patients determined was the optical density of the alveolar process bone tissue from the medial and distal sides of the root of the following teeth 1.6, 1.7, 2.7, 2.6, 3.6, 3.7, 4.7, 4.6, 1.1, 3.1 (the teeth numbers have been recommended by the World Health Organization in order to determine the index of treatment needs of the periodontal disease), and studied were its changes depending on the severity of periodontal disease. Statistical analysis was performed using computer programs «Microsoft Excel», «Biostatistica». Results. In periodontal disease noted was a reduction in the optical density of bone tissue of the alveolar processes of the jaws with a firm relashionship with the severity of disease. In chronic generalized catarrhal gingivitis of moderate severity the optical bone density ranged from 40.445±1.264 to 633.744±5.226 arbitrary units, in mild forms of chronic generalized periodontitis - from -119.664±1.511 to 344.972±4.019, in moderate forms of chronic generalized periodontitis - from -232.589±3.088 to 203.841±1.604, in severe chronic generalized periodontitis - from -464.080±2.398 to -53.991±1.435 arbitrary units. Conclusion. Changes in optical density of bone tissue of the alveolar process of the jaws is an objective criterion for evaluating the status of periodontal tissues, an important diagnostic feature, which also makes it possible to predict the course of the disease and monitor the effectiveness of treatment.

Advancements in the knowledge of induced tooth movement: idiopathic osteosclerosis, cortical bone and orthodontic movement

Moving teeth orthodontically through the dense trabecular bone and cortical areas may require a reduction in the intensity and/or concentration of the applied forces. In part, the orthodontic applied forces are dissipated and reduced by bone deflection, which normally occurs by a slight degree of elasticity of bone tissue in normal conditions. In areas of dense trabecular and in cortical bone this deflection should be insignificant or nonexistent. If there is no reduction in the intensity of the forces in these mentioned regions, the entire force will focus on the structure of the periodontal ligament, increasing the risk of death of cementoblasts, hyalinization and root resorption. Further studies could assess the prevalence of these consequences in populations selected for this purpose, so that would no longer be randomly observed notes.

Structure of COX-1 and COX-2 enzymes and their interaction with inhibitors.

Cyclooxygenase (COX) is the central enzyme in the biosynthetic pathway to prostaglandins (PGs) from arachidonic acid (AA). This protein was purified more than 20 years ago and cloned in 1988. A few years later another protein with COX activity was identified and called COX-2. Although the isoforms of COX are derived from different genes of different size and give rise to distinct mRNA sequences, the proteins are highly homologous in sequence and in three-dimensional structure. They also contain the same two catalytic sites, a peroxidase and a COX site, use the same substrate, AA, and form the same product. The detailed structures of the active COX sites in the isoforms are almost identical. Nevertheless, there are very important biological differences between COX-1 and COX-2. The latter is a highly inducible protein, absent from most tissues in normal conditions but increasing rapidly in response to inflammatory stimuli such as bacterial endotoxin, cytokines, or growth factors. Furthermore, there are differences in substrate binding and, particularly, in inhibitor binding sites that allow the isoforms to be inhibited differentially. This difference is therapeutically significant and selective inhibitors of COX-2 exhibit antiinflammatory potency without the gastric and renal toxicities of the aspirin-like drugs. Selective COX-2 inhibitors may also have important effects on cell growth, development, or survival, reflecting the location of COX-2 on the nuclear membrane of cells. Although much is known of the structure of the isoforms, all the questions have not yet been answered. The new therapeutic possibilities offered by selective inhibitors of COX-2 will encourage a continuing and more detailed analysis of the structures and functions of these closely related proteins.

The “rejection reaction” is not confined solely to the allograft

The rejection process refers primarily to the destruction of foreign tissues by host immune mechanisms. This process affects host lymphoid tissue profoundly and alters the migration patterns of lymphocytes in recipients of organ allografts [8]. It has been shown that specifically sensitized lymphocytes traffic both to and from the transplant [9, 10]. A considerable amount of knowledge has been gathered on the preferential migration pathways of lymphocytes through lymphoid and mucosa-associated lymphoid organs [1, 15]. The factors regulating lymphocyte migration through non-lymphoid tissue in normal conditions are not well known and even less well understood in the context of graft rejection. In this article we described for the first time migration in a recipient non-lymphoid organ (heart) and it's potentially harmful effects in causing parenchymal damage during renal allograft rejection in the rat model. These lesions were detected during the process of developing a model of chronic renal allograft rejection. The pathogenesis of these cardiac lesions is not fully understood but possible mechanisms include upregulation of homing receptors/adhesion molecules, breakdown of peripheral tolerance and involvement of cross-reacting anti-endothelial antibodies.

Aspects of the regulation of glucose transport in insulin-sensitive tissues in normal conditions and in type-2 diabetes

Aspects of the regulation of glucose transport in insulin-sensitive tissues in normal conditions and in type-2 diabetes

Blood appearance of rat alkaline phosphatase originating from the duodenum in vitro

The major source of rat serum alkaline phosphatase (ALP) is well known to be from the intestinal enzyme, but it is still unclear whether it is from the duodenal or the ileal enzyme. The organic origin was investigated by means of two-dimensional electrophoresis. Major isoelectric points and molecular masses for activities of duodenal enzyme treated with both phosphatidylinositol-specific phospholipase C and neuraminidase were identified apparently with those of the major serum enzyme. In organ culture, the normal duodenal enzyme was released in the highest amounts to the culture medium. These results indicate that the major source of serum ALP in adult rats is basically from the duodenal enzyme. On the other hand, lectin affinity chromatography for ALPs showed that the ALP in the medium from culture duodenum and liver had the same complex-type sugar chain as with the ALP in the duodenal tissue. Although the duodenal ALP induced by glucosamine in vitro had the hybrid-type chain, sugar chains of the induced ALP in the culture medium were of the complex type, indicating that medial ALPs possessing the same sugar chain as the native duodenal enzyme, complex type, are mainly released from their tissues in normal conditions.

Conversion of palmitate to respiratory carbon dioxide by foetal tissue of man and monkey.

ALTERATION in the amount of fat deposition in the foetus is clinically well documented for anencephalic, diabetic and low-birth weight infants1–3 and indicates that the rates of synthesis and degradation of foetal lipids, like those of the adult, are influenced by environmental and hormonal factors. It also suggests that the human foetus anabolizes or catabolizes lipids at different rates in response to pathological conditions of gestation. Observations in man and rabbit have shown that the foetus anabolizes lipids essentially from carbohydrate precursors and does not apparently catabolize lipids4,5. If this is true, fatty acids would not be catabolized to respiratory carbon dioxide (CO2) by foetal tissue in normal conditions. The assumption is open to question because slices of human foetal liver incubated with labelled fat have been shown to metabolize this substrate to respiratory carbon dioxide7.

Sudanophilic inclusions in the macrophages in impressions of rats' lung tissue in normal conditions, in alimentary fat loading, and in experimental silicosis

Sudanophilic inclusions in the macrophages in impressions of rats' lung tissue in normal conditions, in alimentary fat loading, and in experimental silicosis