MODELING OF THE SANOGENETIC DEVELOPING ENVIRONMENT AND STARTING NON-DRUG HABILITATION OF PREMATURE INFANTS

The review presents modern data on postnatal adaptation in infants born prematurely, which are characterized by “catching up” the pace of development. It is shown that the conditionally early neonatal period in extremely immature infants can stretch up to 3-4 months of the postnatal life, which is associated with a high risk of adaptation failures with inadequate environmental influences, but at the same time is the basis for a mild aimed correction of perinatal brain damage. Functionally immature structures of the central nervous system of a premature baby were been established to have pronounced plasticity, which can be considered as the ability of the nervous system of a growing organism to reorganize. Plasticity of the nervous system is associated with increased expression of a large complex of neurotrophic biologically active compounds - protein and peptide growth factors of nervous tissue, which intensify the growth and development of nerve cells. At the early stages of the development, changes in the microenvironment of the child and the environment can change the morphofunctional properties of the central nervous system, the rate of psychomotor development, and the behavior of the newborn too significantly. The urgency of the problem is associated with a high incidence of disability in infants born prematurely, as well as with the undesirability of drug loading on an immature organism. The effectiveness of new methods of physical treatment, including weightlessness modeling and positional therapy, as well as the need for active participation of the family in the process of child rehabilitation and in creating a sensory-developing environment, is presented.

Zinc and Copper with New Triazine Hydrazone Ligand: Two Novel Organic Complexes Enhanced Expression of Peptide Growth Factors and Cytokine Genes in Weaned V-Line Rabbit

Two novel transitional organic Zn/Cu complexes based on a new biocompatible bidentate triazine–hydrazone ligand (Thz) was designed, synthesized, and evaluated in this study. This study evaluated the effects of injecting 60 mg of Zn and 40 mg of Cu in three different forms, twice per week, for eight weeks on growth performance, expression of growth factors and cytokine genes, carcass yield, blood biochemicals, and intestinal morphology in weaned rabbits. The tested complexes were sulfate (Cu/ZnSO4), montmorillonite (Cu/Zn-Mnt), and triazine hydrazone (Cu/Zn-Thz). A total of 60 V-line weaned rabbits at four weeks of age were assigned to four treatments (n = 15), which were intramuscularly injected with 0.5 mL of either (1) saline (control) or saline containing (2) Cu/ZnSO4, (3) Cu/Zn-Mnt, or (4) Cu/Zn-Thz. Compared to the controls, the rabbits injected with Cu/Zn-Thz showed a higher (p < 0.01) growth rate, carcass yield (p < 0.05), and liver expression of insulin like growth factor-1 (IGF-1), growth hormone receptor (GHR), fibroblast growth factor-1 (FGF1), and transforming growth factor beta-1 (TGFB1) (p < 0.05), as well as better jejunum morphometric variables (p < 0.05). On the other hand, mRNA of FGF1, TGF1, TCIRG1, and adenosine deaminase (ADA) were higher expressed (p < 0.05) in the spleen tissues of Cu/Zn-Mnt group. Collectively, the results indicated that our novel synthesized organic complexes of Zn/Cu-Thz proved to be a suitable feed supplement, as it increased rabbit productive performance through enhancing expression of peptide growth factors and cytokine genes.

Peptide growth factors and their receptors in the vein wall

The varicose vein wall remodeling is a very complex process, which is controlled by numerous factors, including peptide growth factors. The aim of the study was to assess a/b FGF, IGF-1, TGF-β1, VEGF-A and their receptors in the vein wall. Varicose vein samples were taken from 24 patients undergoing varicose vein surgery. The control material consisted of vein specimens collected from 12 patients with chronic limb ischemia. Contents of aFGF, bFGF, IGF-I, TGF-β1, VEGF, IGF-1R, VEGF R1 and VEGF R2 were assessed with ELISA method. Protein expression of FGF R1 and TGF-β RII were evaluated with western blot. Increased contents of aFGF, IGF-1 and VEGF-A were found in varicose veins in comparison with normal ones (p<0.05). In contrast, a significant decrease in TGF-β content was demonstrated in varicose veins (p<0.05). Furthermore, there was no difference in bFGF content in both groups (p>0.05). IGF-1 R content was significantly increased in varicose veins (p<0.05). There was no difference in VEGF R1 content between varicose and normal veins (p>0.05), whereas VEGF R2 content was significantly increased in varicose veins (p<0.05). Western blot demonstrated increased expression of TGF-β RII in varicose veins (p<0.05) and similar expression of FGF R1 in both groups (p>0.05). Demonstrated changes in peptide growth factors and their receptors may disturb metabolism of extracellular matrix in the varicose vein wall and contribute to the development of the disease to its more advanced stages.

Advancement in Molecular Genetics to understand the molecular reproduction of Livestock – follicular development

Follicular development in the mammalian ovary is a complex process which is potentially regulated by an orchestrated action of the pituitary gonadotropins, e.g., follicle stimulating hormone (FSH) and luteinizing hormone (LH), and local ovarian factors, such as peptide growth factors and steroids. Along with hormonal activation it is necessary to have tight coordination of expression of genes during follicular development. This review highlights the structure and function of ovary, follicle and follicular development. This review also confirms the temporal and spatial expression of the specific genes and miRNAs and their involvement in different modulators, the synthesis of active factors, their interactions, and the dynamics of their receptors on the follicular cell surface may be the ultimate determinants of cellular events which are crucial to coordinated growth and differentiation of follicular cells leading to folliculogenesis and ovulation. DOI: http://dx.doi.org/10.3329/ralf.v1i1.22355 Res. Agric., Livest. Fish.1(1): 47-60, Dec 2014

Recent Insights in the Paracrine Modulation of Cardiomyocyte Contractility by Cardiac Endothelial Cells

The cardiac endothelium is formed by a continuous monolayer of cells that line the cavity of the heart (endocardial endothelial cells (EECs)) and the luminal surface of the myocardial blood vessels (intramyocardial capillary endothelial cells (IMCEs)). EECs and IMCEs can exercise substantial control over the contractility of cardiomyocytes by releasing various factors such as nitric oxide (NO)viaa constitutive endothelial NO-synthase (eNOS), endothelin-1, prostaglandins, angiotensin II, peptide growth factors, and neuregulin-1. The purpose of the present paper is actually to shortly review recent new information concerning cardiomyocytes as effectors of endothelium paracrine signaling, focusing particularly on contractile function. The modes of action and the regulatory paracrine role of the main mediators delivered by cardiac endothelial cells upon cardiac contractility identified in cardiomyocytes are complex and not fully described. Thus, careful evaluation of new therapeutic approaches is required targeting important physiological signaling pathways, some of which have been until recently considered as deleterious, like reactive oxygen species. Future works in the field of cardiac endothelial cells and cardiac function will help to better understand the implication of these mediators in cardiac physiopathology.

CIIA functions as a molecular switch for the Rac1-specific GEF activity of SOS1

Son of sevenless 1 (SOS1) is a dual guanine nucleotide exchange factor (GEF) that activates the guanosine triphosphatases Rac1 and Ras, which mediate signaling initiated by peptide growth factors. In this paper, we show that CIIA is a new binding partner of SOS1. CIIA promoted the SOS1–Rac1 interaction and inhibited the SOS1–Ras interaction. Furthermore, CIIA promoted the formation of an SOS1–EPS8 complex and SOS1-mediated Rac1 activation, whereas it inhibited SOS1-mediated activation of Ras. Transforming growth factor β (TGF-β) up-regulated the expression of CIIA and thereby promoted the association between CIIA and SOS1 in A549 human lung adenocarcinoma cells. Depletion of CIIA in these cells by ribonucleic acid interference inhibited the TGF-β–induced interaction between SOS1 and EPS8, activation of Rac1, and cell migration. Together, these results suggest that CIIA mediates the TGF-β–induced activation of SOS1–Rac1 signaling and cell migration in A549 cells. They further show that CIIA functions as a molecular switch for the GEF activity of SOS1, directing this activity toward Rac1.