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The neonatal period represents a transition phase from the sheltered intrauterine to the exposed extrauterine environment. Changes in haematological profile in five pairs of twin kids and their dams were investigated over a month after the birth. During that period red blood cells (RBC), white blood cells (WBC), haemoglobin (Hb), haematocrit (Hct), mean corpuscular volume (MCV), mean cell haemoglobin (MCH), mean cell haemoglobin concentration (MCHC) and platelets (PLT) level were determined in all animals. Two-way ANOVA showed an increase in RBC (P<0.001), WBC (P<0.0001), MCV (P<0.0001), MCHC (P<0.0001) and PLT (P<0.001). Knowledge of the blood physiological reference values in goat kids provides information useful for the diagnosis and treatment of some neonatal diseases and contributes to recognizing the adaptation mechanisms developing over their first month of life.
Vitamin D-binding protein (DBP) participates in the actin scavenger system, it is a carrier of vitamin D and its derivatives, it manifests the capacity to bind mainly monounsaturated and saturated fatty acids, it binds to the surface of several cells and enhances chemotactic activity of C5a of the complement. The present study was aimed at answering the question whether serum DBP level in mares is related to levels of this protein in colostrum and in serum of its progeny. For this purpose, sera from 77 mares, colostra from 72 mares and sera from 69 Thoroughbred foals were collected. Mother’s age, number of deliveries experienced in the past, month of delivery, feeding of foals with colostra were recorded. Blood of the foals was sampled from the umbilical vein during delivery (0h) and 36-48 h after delivery from the external jugular vein, colostra of the mares were obtained after delivery and blood of the mares was sampled 36-48 h after delivery. Concentration of DBP was estimated by a self-designed ELISA. In the present study, DBP concentrations in newborn’s serum were found independent of their concentrations in mother’s serum, her age and number of parities experienced in the past. Colostrum DBP level was found to be lower than that in the mare’s serum and was not correlated to the concentration of this protein in mare’s serum. There was no effect of colostrum feeding on DBP level in the foal serum. These results indicate that serum DBP concentration in newborn foals depends on factors which act directly on the foal. Because of the lack of correlation between plasma and colostrum concentrations of DBP, it can be assumed that DBP is synthesised in the mammary gland and/or specific transport mechanisms exist in the mammary gland.
During the neonatal period of life, hypoxia appears as a major risk factor which may result in complex cerebral dysfunctions like cerebral palsy or seizure disabilities. Natural neuroprotection against hypoxia-induced injury in females is considered to be due to the effects of circulating ovarian hormones, which are lost after ovariectomy or reproductive senescence. Although anti-hypoxic effects of estrogen have been documented, its clinical use has certain limitations. Selective estrogen receptor modulators (SERMs) and selective aryl hydrocarbon receptor modulators (SAhRs) may act as receptor agonists or antagonists in a tissue-specific manner, thus representing a novel approach for the treatment or the prevention of various types of neural degeneration and seizures. In this study we evaluated the mechanism of action of raloxifene and 3,3’-diindolylmethane (DIM) in response to hypoxia in mouse embryonic neuronal cells in primary cultures. Raloxifene is known to bind to estrogen receptors with SERM properties, whereas (DIM) exhibits properties of SAhRs. In our study, hypoxic conditions (5% CO2/95% nitrogen) induced caspase-3 activity and lactate dehydrogenase (LDH) release in the hippocampal cell cultures. Raloxifene and DIM inhibited the hypoxia-induced LDH release by 10–51% and 9–61%, respectively. DIM inhibited also the hypoxia-induced caspase-3 activity by 2–18%, but raloxifene did not affect the hypoxia-induced apoptotic parameter. In our model of hypoxia, estrogen receptor alpha (ER alpha) antagonist MPP (0.01 µM) did not reverse raloxifene-mediated neuroprotection. However, a high-affinity estrogen receptor beta (ER beta) antagonist, PHTPP (0.01 μM), and G-protein coupled receptor 30 antagonist (GPR30), G-15 (0.01 µM), enhanced the neuroprotective effects of raloxifene, which point to neurotoxic potential of ER beta and GPR30 activation in hypoxia. Selective antagonist of aryl hydrocarbon receptors (AhR) alpha-naphthoflavone (1 µM) did not influence neuroprotective action of DIM, thus suggesting AhR-independent effect. These data demonstrated strong neuroprotective potential of raloxifene and DIM which may represent novel therapeutic tools for brain exposed to hypoxic insults. This study was supported by the Polish National Center of Science grant No 2011/01/N/NZ3/04786
Mesenchymal stem cells (MSC) exert unique ability to differentiate into various cells of mesodermal origin. These properties place MSC as a very promising source of cells for regenerative medicine and tissue engineering. Recently, it has been shown that experimental transplantation of MSC improves a variety of neurological dysfunctions. Bone marrow (BM) represents the mostly exploited source of human therapeutic stem cells but similar populations have been recently identified in many other tissues and organs. Among them umbilical cord Wharton jelly (WJ) has been recognized for its safety, accessibility and differentiation potential. This study compares human Wharton jelly-derived MSC (WJ-MSC) and human bone marrow-derived MSC (BM-MSC) in terms of cell phenotype, optimal growth and multilineage differentiation characteristics with special attention to neurogenic potential demonstrated by both type of cells. Materials and Methods: MSC were isolated from human Wharton jelly and human bone marrow then cultured in vitro in Lonza medium in defined conditions. Then both cell types were subjected to the specific induction media (Gibco) to analyze their potential to differentiate into osteo-, chondro- adipo- and myogenic lineages. Transcriptional activity of genes characteristic for early and late stages of cell differentiation has been examined using RT-PCR. Concomitantly immunochemical analysis of certain gene-related proteins has been performed by immunocytochemical methods. Results: We have demonstrated that both isolated WJ-MSC and BM-MSC exhibited characteristic, mesenchymal cell specific phenotypes by expressing the panels of surface antigens (CD73, CD90, CD105, CD166) as well as typical for MSC multilineage differentiation markers. However, efficiency of these processes differs markedly between the cells derived from each of examined tissues. Thus, WJ-MSC appeared to be much less prone to adipogenic differentiation in comparison to BM-MSC. In contrast, WJMSC revealed higher proliferation and neural differentiations potential than BM-MSC. Consistently, only WJ-MSC-derived cells unveiled neural progenitor characteristics expressing panel of cellular markers typical for neural lineage differentiation, i.e. Nestin, NF200, GFAP. All together, these data allow us to hypothesize that the fetal origin of WJ tissue determines its distinguished neuro-mesenchymal characteristic. This is consisted with the data of Takashima et al. (2007) showing that neonatal MSC cultures contain substantially high number of cells being descendants of the earliest wave of developmentally discern neuroepithelial MSC lineage derived from cranial part of neural crest and clearly partitioned from MSC residing in adult bon marrow niche. Conclusions: The study demonstrated that WJ-MSC, similarly to BM-MSC, can be effectively expanded in culture up to 6–8 passages when maintaining cells in undifferentiated state expressing common MSC markers. In contrast, the both MSC lines differ markedly in their ability to lineage differentiation. The most striking difference was that only WJ-MSC can be induced to neural phenotypes. Consisted with this observation WJMSC seems to be more favorable than BM-MSC to cell replacement therapy of neurodegenerative diseases. Supported by NSC grant No 2011/01/B/NZ3/0540
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