Gotowe bibliografie tematyczne / Blood proteins Physiology

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Gotowa bibliografia na temat „Blood proteins Physiology”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 29 stycznia 2023

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Artykuły w czasopismach na temat "Blood proteins Physiology"

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Davies, Peter L., Choy L. Hew i Garth L. Fletcher. "Fish antifreeze proteins: physiology and evolutionary biology". Canadian Journal of Zoology 66, nr 12 (1.12.1988): 2611–17. http://dx.doi.org/10.1139/z88-385.

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Many marine teleosts have adapted to ice-laden seawater by evolving antifreeze proteins and glycoproteins. These proteins are synthesized in the liver for export to the blood where they circulate at levels of up to 20 mg/mL. There are at least four distinct antifreeze protein classes differing in carbohydrate content, amino acid composition, protein sequence, and secondary structure. In addition to antifreeze structural diversity, fish species differ considerably with respect to mechanisms controlling seasonal regulation of plasma antifreeze concentrations. Some species synthesize antifreeze proteins immediately before the onset of freezing conditions, some synthesize them in response to such conditions, whereas others possess high concentrations all year. Endogenous rhythms, water temperature, photoperiod, and pituitary hormones have all been implicated as regulators of plasma antifreeze protein levels. The structural diversity of antifreeze proteins and their occurrence in a wide range of fish species suggest that they evolved separately and recently during Cenozoic glaciation. Invariably, the genes coding for these antifreeze proteins are amplified, sometimes as long tandem arrays, suggesting intense selective pressure to produce large amounts of protein. The distribution of antifreeze gene types among fish species suggests that they could serve as important tools for studying phylogenetic relationships.
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Jia, Ruizhe, Jingyun Li, Can Rui, Hui Ji, Hongjuan Ding, Yuanqing Lu, Wei De i Lizhou Sun. "Comparative Proteomic Profile of the Human Umbilical Cord Blood Exosomes between Normal and Preeclampsia Pregnancies with High-Resolution Mass Spectrometry". Cellular Physiology and Biochemistry 36, nr 6 (2015): 2299–306. http://dx.doi.org/10.1159/000430193.

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Background/Aims: Exosomes are extracellular vesicles that are involved in several biological processes. The roles of proteins from human umbilical cord blood exosomes in the pathogenesis of preeclampsia remains poorly understood. Methods: In this study, we used high-resolution LC-MS/MS technologies to construct a comparative proteomic profiling of human umbilical cord blood exosomes between normal and preeclamptic pregnancies. Results: A total of 221 proteins were detected in human umbilical cord blood exosomes, with 14 upregulated and 15 downregulated proteins were definitively identified between preeclamptic and control pregnancies. Further bioinformatics analysis (Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis) indicated that these differentially expressed proteins correlate with enzyme regulator activity, binding, extracellular region, cell part, biological regulation, cellular process and complement and coagulation cascades occurring during pathological changes of preeclampsia. Conclusion: Our results show significantly altered expression profiles of proteins in human umbilical cord blood exosomes between normal and preeclampsia pregnancies. These proteins may be involved in the etiology of preeclampsia.
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Croxatto, HR. "How Many Peptidic Hormones Can Derive From Blood Plasma Proteins?" Physiology 5, nr 5 (1.10.1990): 201–4. http://dx.doi.org/10.1152/physiologyonline.1990.5.5.201.

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Peptides having structures identical or related to some already known hormones have been obtained using pepsin as a hydrolytic agent acting at acid pH upon plasma substrates. The data suggest the existence of systems similar to renin-angiotensin for the generation of active peptides other than angiotensin or kinins.
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Ohno, H., K. Yamashita, R. Doi, K. Yamamura, T. Kondo i N. Taniguchi. "Exercise-induced changes in blood zinc and related proteins in humans". Journal of Applied Physiology 58, nr 5 (1.05.1985): 1453–58. http://dx.doi.org/10.1152/jappl.1985.58.5.1453.

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Effects of cycle ergometer exercise (approximately 75% maximum ventilatory O2 consumption for 30 min) on the concentrations of zinc and related proteins in erythrocytes and/or plasma were studied on 11 sedentary male students. Lower concentrations of total zinc and of zinc derived from carbonic anhydrase I type (CA-I) in erythrocytes were observed immediately after exercise, but they disappeared after 30 min of rest. The change in total zinc concentration in erythrocytes correlated well with that in CA-I concentration immediately after exercise, as well as after rest. The concentration of carbonic anhydrase II type (CA-II)-derived zinc did not vary substantially at any time. On the other hand, there were significant increases in the plasma concentrations of total zinc and of alpha 2-macroglobulin (alpha 2-MG)-bound zinc immediately after exercise, whereas no such effect was noted in albumin-bound zinc. A positive correlation was found between total zinc and alpha 2-MG concentrations in plasma immediately after exercise. In addition, the change in the activity of alkaline phosphatase, a zinc metalloenzyme, correlated well with that in the total zinc concentration in plasma. These results suggest that a brief physical exercise induces the movement of zinc into plasma.
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Teahan, Carmel G., Hugh A. McKenzie i Mervyn Griffiths. "Some monotreme milk “whey” and blood proteins". Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 99, nr 1 (styczeń 1991): 99–118. http://dx.doi.org/10.1016/0305-0491(91)90014-5.

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Richardson, Samantha J., Julie A. Monk, Caroline A. Shepherdley, Lars O. E. Ebbesson, Frank Sin, Deborah M. Power, Peter B. Frappell, Josef Köhrle i Marilyn B. Renfree. "Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, nr 5 (maj 2005): R1264—R1272. http://dx.doi.org/10.1152/ajpregu.00793.2004.

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Thyroid hormones are essential for vertebrate development. There is a characteristic rise in thyroid hormone levels in blood during critical periods of thyroid hormone-regulated development. Thyroid hormones are lipophilic compounds, which readily partition from an aqueous environment into a lipid environment. Thyroid hormone distributor proteins are required to ensure adequate distribution of thyroid hormones, throughout the aqueous environment of the blood, and to counteract the avid partitioning of thyroid hormones into the lipid environment of cell membranes. In human blood, these proteins are albumin, transthyretin and thyroxine-binding globulin. We analyzed the developmental profile of thyroid hormone distributor proteins in serum from a representative of each order of marsupials ( M. eugenii; S.crassicaudata), a reptile ( C. porosus), in two species of salmonoid fishes ( S. salar; O. tshawytsch), and throughout a calendar year for sea bream ( S. aurata). We demonstrated that during development, these animals have a thyroid hormone distributor protein present in their blood which is not present in the adult blood. At least in mammals, this additional protein has higher affinity for thyroid hormones than the thyroid hormone distributor proteins in the blood of the adult. In fish, reptile and polyprotodont marsupial, this protein was transthyretin. In a diprotodont marsupial, it was thyroxine-binding globulin. We propose an hypothesis that an augmented thyroid hormone distributor protein network contributes to the rise in total thyroid hormone levels in the blood during development.
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Synelnyk, T. B., O. O. Kravchenko, O. S. Kostiuk, O. M. Savchuk, S. A. Sukhodolia i L. I. Ostapchenko. "DISTRIBUTION OF SERINE PROTEASES IN BLOOD PLASMA AND PANCREAS IN CHRONIC PANCREATITIS AND ONCOPATHOLOGY". Fiziolohichnyĭ zhurnal 68, nr 6 (8.12.2022): 31–43. http://dx.doi.org/10.15407/fz68.06.031.

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The aim of our study was to evaluate the trypsin-like serine proteases (TLPs) distribution between systemic circulation and pancreatic tissue and to investigate the peculiarities of their involvement in the extracellular matrix components degradation in patients with pancreatic pathologies with electrophoretic analysis methods using. Тhe Khmelnitsky Regional Clinical Hospital patients aged 28-89 were selected for this study: 20 people with chronic pancreatitis (group CP); 20 people with pancreatic cancer (group PC); 20 conditionally healthy persons (control). Blood plasma samples and pancreatic tissue homogenates were obtained from all the patients, from which the TLPs fractions were subsequently obtained by the affinity chromatography method. The study showed that TLPs content in the blood plasma of patients with pancreatic pathologies is higher, and in tissue homogenates is lower relative to the values of the corresponding indicators in the control. Disk-electrophoresis using showed that TLPs fractions obtained from the blood plasma of patients of all studied groups contain a lot of high molecular weight (HMW) proteins, while TLPs from the pancreatic tissue homogenates of patients with pancreatic pathologies mainly consists of low molecular weight (LMW) proteins. Enzyme-electrophoresis results showed that all TLPs fractions include enzymes with fibrinogenolytic, gelatinolytic and collagenolytic activity. In plasma, the first were represented by medium molecular weight (MMW) proteins, and the last two groups included a lot of HMW proteins as well as proteins with very high molecular weight. In homogenates, fibrinogenolytic activity was characteristic for LMW proteins only, whereas gelatinases and collagenases were represented by both MMW and LMW proteins. Our results indicate the differences in the TLPs fractions components obtained from blood plasma and pancreatic tissue of patients with investigated pathologies, as well as significant distinctions in the processes of extracellular matrix remodeling under СР and РС.
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Lampe, L., K. Wienhold, G. Meyer, F. Baisch, H. Maass, W. Hollmann i R. Rost. "Effects of simulated microgravity (HDT) on blood fluidity". Journal of Applied Physiology 73, nr 4 (1.10.1992): 1366–69. http://dx.doi.org/10.1152/jappl.1992.73.4.1366.

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Exposures to microgravity and head-down tilt (HDT) produce similar changes in body fluid. This causes an increase in hematocrit that significantly affects hemorheological values. Lack of physical stimulation under bed rest conditions and the relative immobility of the crew during spaceflight also affects the blood fluidity. A group of six healthy male subjects participated as volunteers, and blood samples were collected 10 days before, on day 2 and day 9, and 2 days after the HDT phase. Blood rheology was quantified by plasma viscometry, red cell aggregability, and red cell deformability. A reduced red cell deformability, an indication of the diminished quality of the red blood cells, was measured under HDT conditions that finally led to the so-called “space flight anemia.” Enhanced red cell membrane fragility induced by diminished physical activity and an increase in hemoglobin concentration are responsible for this effect. Plasma viscosity is reduced as a result of diminished plasma proteins. However, despite the reduction in plasma proteins, including fibrinogen, alpha 2-macroglobulin, and immunoglobulin M, red cell aggregation was enhanced, principally because of the increase in hematocrit. Our results of hemorheological alterations under HDT conditions may help to elucidate the formerly documented hematologic changes during spaceflight.
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Martino, Tami A., Nazneen Tata, Georg A. Bjarnason, Marty Straume i Michael J. Sole. "Diurnal protein expression in blood revealed by high throughput mass spectrometry proteomics and implications for translational medicine and body time of day". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, nr 3 (wrzesień 2007): R1430—R1437. http://dx.doi.org/10.1152/ajpregu.00183.2007.

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Molecular gene cycling is useful for determining body time of day (BTOD) with important applications in personalized medicine, including cardiovascular disease and cancer, our leading causes of death. However, it impractically requires repetitive invasive tissue sampling that is obviously not applicable for humans. Here we characterize diurnal protein cycling in blood using high-throughput proteomics; blood proteins are easily accessible, minimally invasive, and can importantly serve as surrogates for what is happening elsewhere in the body in health and disease. As proof of the concept, we used normal C57BL/6 mice maintained under regular 24-h light and dark cycles. First, we demonstrated fingerprint patterns in 24-h plasma, revealed using surface-enhanced laser desorption and ionization (SELDI). Second, we characterized diurnal cycling proteins in blood using chromatography and tandem electrospray ionization mass spectrometry. Importantly, we noted little association between the cycling blood proteome and tissue transcriptome, delineating the necessity to identify de novo cycling proteins in blood for measuring BTOD. Furthermore, we explored known interaction networks to identify putative functional pathways regulating protein expression patterns in blood, thus shedding new light on our understanding of integrative physiology. These studies have profound clinical significance in translating the concept of BTOD to the practical realm for molecular diagnostics and open new opportunities for clinically relevant discoveries when applied to ELISA-based molecular testing and/or point-of-care devices.
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van de Graaf, Stan F. J., Joost G. J. Hoenderop i René J. M. Bindels. "Regulation of TRPV5 and TRPV6 by associated proteins". American Journal of Physiology-Renal Physiology 290, nr 6 (czerwiec 2006): F1295—F1302. http://dx.doi.org/10.1152/ajprenal.00443.2005.

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The epithelial Ca2+ channels TRPV5 and TRPV6 are the most Ca2+-selective members of the TRP channel superfamily. These channels are the prime target for hormonal control of the active Ca2+ flux from the urine space or intestinal lumen to the blood compartment. Insight into their regulation is, therefore, pivotal in our understanding of the (patho)physiology of Ca2+ homeostasis. The recent elucidation of TRPV5/6-associated proteins has provided new insight into the molecular mechanisms underlying the regulation of these channels. In this review, we describe the various means of TRPV5/6 regulation, the role of channel-associated proteins herein, and the relationship between both processes.
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Rozprawy doktorskie na temat "Blood proteins Physiology"

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Su, Linlin, i 苏琳琳. "Drug transporters and blood-testis barrier dynamics". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47752816.

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Bexis, Sotiria. "The relationship between vascular structure, contractile proteins, vascular reactivity and blood pressure in animal models of hypertension /". Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phb572.pdf.

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Mwaikambo, Bupe Rose. "Emerging roles for the CD36 scavenger receptor in neovascular ocular disease". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115899.

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Ocular neovascularization (NV) associated with corneal NV, ischemic retinopathies and age-related macular degeneration is a leading cause of severe vision loss. While numerous contributing factors have been identified, the potential role of the CD36 scavenger receptor has been largely overlooked notwithstanding its crucial involvement in normal retinal function. Accordingly, the central aim of this work was to elucidate the contribution and regulation of CD36 during ocular NV using the cornea as a model.
Initial work investigating the role of CD36 10 maintaining corneal avascularity, an important feature of the normal cornea, revealed that genetic ablation of CD36 elicits age-related corneal NV. Subsequent studies using a pathophysiologically relevant model of inflammatory corneal NV showed constitutive expression of CD36 in the normal cornea with marked induction in the neovascularized cornea. Importantly, activation of CD36 suppressed and induced regression of corneal NV, effects that proceeded via concerted inhibition of VEGFA, JNK-1, and cJun.
Because hypoxia is a fundamental stimulus for angiogenesis, it was pertinent to explore the role and regulation of CD36 during hypoxia. We demonstrate that CD36 expression was significantly elevated in hypoxia-exposed corneal and retinal tissue and in hypoxic retinal pigment epithelial cells. Essential contributions of hypoxia-inducible factor (HIF)-1 and reactive oxygen species were also established. Functional consequences were depicted by augmentations in CD36 phagocytic and anti-angiogenic activities.
Collectively, data disclose CD36 as an important modulator of corneal avascularity and inflammatory corneal NV; this imparts several interesting avenues for future research on the involvement of CD36 in neovascular diseases of the eye. Novel data further identify CD36 as a hypoxia and HIF-1 regulated gene thus creating a framework for future elucidation of the regulatory aspects of this receptor.
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Jiang, Liying. "Exposure of endothelial cells to shear stress stimulates protein tryosine phosphorylation". Thesis, Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25421.

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Liang, Yan, i 梁艳. "Endothelial LKB1/AMPK signaling pathway in regulating energy and vascular homeostasis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193460.

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Liver kinase B1 (LKB1), a serine/threonine kinase, is responsible for the activation of AMP-activated protein kinase (AMPK), the master regulator of energy metabolism. LKB1/AMPK signaling pathway possesses a wide range of biological functions in regulating cell cycle progression, cell polarity, senescence and inflammation. In cultured endothelial cells, the pro-senescence function of LKB1/AMPK signaling pathway has been observed. However, the mechanisms by which LKB1 is regulated in endothelial cells remain largely uncharacterized. Furthermore, little is known about the effects of activated endothelial LKB1/AMPK signaling pathway on vascular and energy homeostasis. The present study aimed to investigate the upstream molecular mechanisms regulating LKB1 protein stability during endothelial senescence and the downstream pathophysiological effects of hyperactivated AMPK signaling in endothelial cells. In cultured model of cellular senescence, the lysine (K) 64 residue of LKB1 was found to be crucial for mediating its pro-senescence activities. The protein stability and intracellular localization of LKB1 mutant with K64 replaced by arginine (R) was different from the wild type protein. K64R exhibited enhanced effects on promoting endothelial senescence. Moreover, mutation of this residue attenuated the binding to HERC2, a newly identified E3 ubiquitin ligase for LKB1, in turn preventing its ubiquitination and degradation. Using a transgenic mouse model that selectively over-expresses a constitutively active AMPK α1 subunit (EC-AMPK) in endothelial cells, the influence of hyperactivated AMPK signaling on metabolic and vascular functions was investigated. Under standard chow condition, the metabolic phenotypes were similar between wild type and EC-AMPK mice; under high fat diet condition, EC-AMPK mice showed more severe obesity-induced fatty liver injury. Selective activation of AMPK in endothelial cells caused vascular and hepatic inflammation. Cyclooxygenase-2 (COX-2) was found to be the mediator for the pro-inflammatory functions of AMPK in vascular endothelial cells and facilitated to the development of obesity-induced fatty liver injury in EC-AMPK mice. Evaluation using isolated arteries revealed an increased systolic blood pressure and abnormal endothelial function in EC-AMPK miceunder high fat diet. AMPK activation in endothelium of the blood vessel could not block vascular remodeling associated with dietary obesity. Taken in conjunction, the above findings suggest that continuous activation of LKB1/AMPK signaling elicits adverse effects on both energy and vascular homeostasis.
published_or_final_version
Pharmacology and Pharmacy
Doctoral
Doctor of Philosophy
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Waghulde, Harshal B. "Mapping and CRISPR/Cas9 Gene Editing for Identifying Novel Genomic Factors Influencing Blood Pressure". University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1470402637.

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Henninger, Nils. "Inhibiting Axon Degeneration in a Mouse Model of Acute Brain Injury Through Deletion of Sarm1". eScholarship@UMMS, 2017. http://escholarship.umassmed.edu/gsbs_diss/900.

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Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly following TBI. Although severe brain injury may cause immediate disruption of axons (primary axotomy), it is now recognized that the most frequent form of traumatic axonal injury (TAI) is mediated by a cascade of events that ultimately result in secondary axonal disconnection (secondary axotomy) within hours to days. Proposed mechanisms include immediate post-traumatic cytoskeletal destabilization as a direct result of mechanical breakage of microtubules, as well as catastrophic local calcium dysregulation resulting in microtubule depolymerization, impaired axonal transport, unmitigated accumulation of cargoes, local axonal swelling, and finally disconnection. The portion of the axon that is distal to the axotomy site remains initially morphologically intact. However, it undergoes sudden rapid fragmentation along its full distal length ~72 h after the original axotomy, a process termed Wallerian degeneration. Remarkably, mice mutant for the Wallerian degeneration slow (Wlds) protein exhibit ~tenfold (for 2–3 weeks) suppressed Wallerian degeneration. Yet, pharmacological replication of the Wlds mechanism has proven difficult. Further, no one has studied whether Wlds protects from TAI. Lastly, owing to Wlds presumed gain-of-function and its absence in wild-type animals, direct evidence in support of a putative endogenous axon death signaling pathway is lacking, which is critical to identify original treatment targets and the development of viable therapeutic approaches. Novel insight into the pathophysiology of Wallerian degeneration was gained by the discovery that mutant Drosophila flies lacking dSarm (sterile a/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously recapitulated the Wlds phenotype. The pro-degenerative function of the dSarm gene (and its mouse homolog Sarm1) is widespread in mammals as shown by in vitro protection of superior cervical ganglion, dorsal root ganglion, and cortical neuron axons, as well as remarkable in-vivo long-term survival (>2 weeks) of transected sciatic mouse Sarm1 null axons. Although the molecular mechanism of function remains to be clarified, its discovery provides direct evidence that Sarm1 is the first endogenous gene required for Wallerian degeneration, driving a highly conserved genetic axon death program. The central goals of this thesis were to determine (1) whether post-traumatic axonal integrity is preserved in mice lacking Sarm1, and (2) whether loss of Sarm1 is associated with improved functional outcome after TBI. I show that mice lacking the mouse Toll receptor adaptor Sarm1 gene demonstrate multiple improved TBI-associated phenotypes after injury in a closed-head mild TBI model. Sarm1-/- mice developed fewer beta amyloid precursor protein (βAPP) aggregates in axons of the corpus callosum after TBI as compared to Sarm1+/+ mice. Furthermore, mice lacking Sarm1 had reduced plasma concentrations of the phosphorylated axonal neurofilament subunit H, indicating that axonal integrity is maintained after TBI. Strikingly, whereas wild type mice exhibited a number of behavioral deficits after TBI, I observed a strong, early preservation of neurological function in Sarm1-/- animals. Finally, using in vivo proton magnetic resonance spectroscopy, I found tissue signatures consistent with substantially preserved neuronal energy metabolism in Sarm1-/- mice compared to controls immediately following TBI. My results indicate that the Sarm1-mediated prodegenerative pathway promotes pathogenesis in TBI and suggest that anti-Sarm1 therapeutics are a viable approach for preserving neurological function after TBI.
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Chakaroun, Rima. "Effects of weight loss and exercise on chemerin serum concentrations and adipose tissue expression in human obesity". Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-158639.

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Chemerin is a chemoattractant adipokine that regulates adipogenesis and may induce insulin resistance. Chemerin serum concentrations are elevated in obese, insulin-resistant, and inflammatory states in vivo. Here we investigate the role of omental (OM) and subcutaneous (SC) adipose tissue chemerin and CMKLR1 messenger RNA (mRNA) expression in human obesity. In addition, we test the hypothesis that changes in chemerin serum concentrations are primarily associated with reduced body fat mass in the context of 3 weight loss intervention studies. Chemerin serum concentration was measured in 740 individuals in a cross-sectional (n = 629) study including a subgroup (n = 161) for which OM and SC chemerin mRNA expression has been analyzed as well as in 3 interventions including 12 weeks of exercise (n = 60), 6 months of calorie-restricted diet (n = 19) studies, and 12 months after bariatric surgery (n = 32). Chemerin mRNA is significantly higher expressed in adipose tissue of patients with type 2 diabetes mellitus and correlates with circulating chemerin, body mass index (BMI), percentage body fat, C-reactive protein, homeostasis model assessment of insulin resistance, and glucose infusion rate in euglycemic-hyperinsulinemic clamps. CMKLR1 mRNA expression was not significantly different between the 2 fat depots. Obesity surgery–induced weight loss causes a significant reduction on both OM and SC chemerin expression. All interventions led to significantly reduced chemerin serum concentrations. Decreased chemerin serum concentrations significantly correlate with improved glucose infusion rate and reduced C-reactive protein levels independently of changes in BMI. Insulin resistance and inflammation are BMI-independent predictors of elevated chemerin serum concentrations. Reduced chemerin expression and serum concentration may contribute to improved insulin sensitivity and subclinical inflammation beyond significant weight loss.
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Julien, Mathéau A. "Mechanical Strain-Mediated Syndecan Regulation and Its Effects on Adhesion of Vascular Smooth Muscle Cells". Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/7007.

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An injured vascular system has a substantial impact on an individuals overall health, and an understanding of the mechanisms that underlie blood vessel pathophysiology is required for the development of rational and effective treatment strategies. The phenotypic modulation of smooth muscle cells (SMC) during vascular injury, characterized by altered adhesion, migration and synthetic behavior, plays an important role in the eventual outcome. Specifically, the ability of SMCs to adhere to and remodel their extracellular environment via regulation of the syndecan class of cell adhesion molecules dictates the response of the vascular wall to local injury. The effect of in vitro syndecan-4 regulation on SMC adhesion was investigated through the use of a glass microsphere centrifugation assay, and an antisense-mediated reduction in gene expression was found to correlate with decreased adhesive strength. Regulation of syndecan-1, syndecan-2, and syndecan-4 gene expression was observed experimentally by mechanical strain of SMCs. Using real-time polymerase chain reaction (PCR), the kinetics of both static and cyclic mechanical strain were found to modify the gene expression in a time and strain magnitude-dependent manner unique to each syndecan. In particular, the responses of syndecan-4 were acute, but transient, while the evolution of syndecan-1 and syndecan-2 regulation was delayed by comparison. Mechanical strain also modulated syndecan-4 protein expression and ectodomain shedding, as measured by Western immunoblotting, and this effect was found, through selective inhibition, to be at least in part dependent on mitogen-activated protein (MAP) kinase signaling. In particular, intact extracellular signal-regulated MAP kinase (ERK) 1/2 and c-Jun NH2-terminal kinase / stress-activated protein kinase (JNK/SAPK) signaling pathways were found to be required for the observed strain-induced shedding. These findings offer a better understanding of syndecan function in response to mechanical strain and suggest potential new mechanisms by which physical forces may modulate vascular SMC behavior and regulation during normal physiology, pathologic conditions, and engineered arterial substitute development.
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Babin, Patrick. "Lipoproteines et apolipoproteines plasmatiques chez les poissons teleosteens". Paris 6, 1987. http://www.theses.fr/1987PA066032.

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Caracterisation des lipoproteines plasmatiques et de leurs apolipoproteines chez salmo gairdneri. Determination de leur masse moleculaire et de leur densite. L'etude au long du cycle annuel de reproduction a permis de demontrer la presence de proteines vitellines ovulaires dans le plasma. De plus, le role des lipoproteines, plasmatiques dans la steroidogenese ovarienne a ete etudie
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Książki na temat "Blood proteins Physiology"

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Andreeva, Alla Michailovna. Structural and functional organization of fish blood proteins. Hauppauge, N.Y: Nova Science, 2011.

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Hepatic plasma proteins: Mechanisms of function and regulation. San Diego: Academic Press, 1993.

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Job, Harenberg, i Heidelberger Akademie der Wissenschaften, red. New trends in haemostasis: Coagulation proteins, endothelium, and tissue factors. Berlin: Springer-Verlag, 1990.

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International, Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells (1989 Fukuoka-shi Japan). Anion transport protein of the red blood cell membrane: Proceedings of the International Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells, Fukuoka, 1-3 May 1989. Amsterdam: Elsevier, 1989.

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1949-, Agre Peter, i Cartron Jean Pierre, red. Protein blood group antigens of the human red cell: Structure, function, and clinical significance. Baltimore: Johns Hopkins University Press, 1992.

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S, Pagano Irwin, i Strait Nathan B, red. HDL and LDL cholesterol physiology and clinical significance. Hauppauge, NY: Nova Science Publishers, 2009.

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R, Harris James, red. Erythroid cells. New York: Plenum Press, 1990.

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Edwin J. Cohn and the development of protein chemistry: With a detalied account of his work on the fractionation of blood during and after World War II. [Boston, Mass.]: Published by Center for Blood Research, Inc., 2002.

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A, Schreiber, red. Primate phylogeny from a human perspective: A study based on the immunological technique of comparative determinant analysis (CDA). Stuttgart: G. Fischer, 1996.

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service), ScienceDirect (Online, red. The HDL handbook: Biological functions and clinical implications. London: Academic, 2010.

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Części książek na temat "Blood proteins Physiology"

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Bauer, C., i W. Wuillemin. "Blood, Plasma Proteins, Coagulation, Fibrinolysis, and Thrombocyte Function". W Comprehensive Human Physiology, 1651–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60946-6_84.

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Ogawa, Kishiko, i Elvira Fehrenbach. "Exercise Intensity and Duration Affect Blood-Soluble HSP72". W Heat Shock Proteins and Whole Body Physiology, 253–65. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3381-9_15.

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Nag, Sukriti, Dan Kilty i Shruti Dev. "Extracellular Matrix Proteins in Cerebral Vessels in Chronic Hypertension". W Biology and Physiology of the Blood-Brain Barrier, 327–31. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_53.

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Stanimirovic, Danica B., Rita Ball, Josée Wong i Jon P. Durkin. "The Role of Protein Kinase C and Marcks Protein Phosphorylation in Rat Cerebromicrovascular Endothelial Cell Proliferation Induced by Astrocyte-Derived Factors". W Biology and Physiology of the Blood-Brain Barrier, 213–20. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_36.

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Calvo, Charles-Félix, i Michel Mallat. "Expression of Macrophage Chemotactic Protein-1 in Rat Glial Cells". W Biology and Physiology of the Blood-Brain Barrier, 271–77. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_44.

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Mannucci, P. M., S. Viganò, S. Antoncecchi i N. Ciavarella. "Protein C — An Inhibitor of Blood Coagulation: Biochemistry, Physiology, Clinical Aspects". W Advances in Hemostasis and Thrombosis, 149–57. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9424-6_15.

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Stanimirovic, Danica B., Paul Morley, Edith Hamel, Rita Ball, Geoff Mealing i Jon P. Durkin. "Calcium and Protein Kinase C Signaling in Response to Vasoactive Peptides in Human Cerebromicrovascular Endothelial Cells". W Biology and Physiology of the Blood-Brain Barrier, 221–27. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_37.

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Passow, Hermann. "Molecular aspects of band 3 protein-mediated anion transport across the red blood cell membrane". W Reviews of Physiology, Biochemistry and Pharmacology, Volume 103, 61–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/3540153330_2.

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Sembulingam, K., i Prema Sembulingam. "Blood and Plasma Proteins". W Essentials of Physiology for Dental Students, 38. Jaypee Brothers Medical Publishers (P) Ltd., 2011. http://dx.doi.org/10.5005/jp/books/11397_6.

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Pramanik, Debasis. "Composition of blood and plasma proteins". W Principles of Physiology, 87. Jaypee Brothers Medical Publishers (P) Ltd., 2015. http://dx.doi.org/10.5005/jp/books/12674_12.

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Streszczenia konferencji na temat "Blood proteins Physiology"

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Comp, P. C., i C. T. Esmon. "Defects in the protein C pathway". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643715.

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Activated protein C functions as an anticoagulant by enzymatically degrading factors Va and Villa in the clotting cascade. Protein C may be converted to its enzymatically active form bythrombin. The rate at which thrombin cleavage of the zymogen occurs is greatly enhanced when thrombin is bound to an endothelial cell receptor protein, thrombomodulin. Activated proteinC has a relatively long half-life in vivo and the formation of activated protein C in response to low level thrombin infusion suggests that the protein C system may provide a feedback mechanism to limit blood clotting. Clinical support for such a physiologic role for activated protein C includes an increased incidence of thrombophlebitis and pulmonary emboli in heterozygous deficient individuals, and severe, often fatal, cutaneous thrombosis in homozygous deficient newborns. A third thrombotic condition associated with protein C deficiency is coumarin induced skin (tissue) necrosis. This localized skin necrosis occurs shortly after the initiation of coumarin therapy and is hypothesized to bedue to the rapid disappearance of protein C activity in the plasma beforean adequate intensity of anticoagulation is achieved. Recent estimates of heterozygous protein C deficiency range as high as 1 in 300 individuals in the general population. Since coumarin compounds are in routine clinical use throughout the world and skin necrosis remains a relatively rare clinical finding, this suggests that factors other than protein C deficiency alone may be involved in the pathogenesis of the skin necrosis.The anticoagulant properties of activated protein C are greatly enhanced by another vitamin K-dependent plasma protein, protein S. Protein S functions by increasing the affinity of activated protein C for cell surfaces.Protein S is found in two forms in plasma: free and in complex with C4b-binding protein, "an inhibitor of the complement system. Free protein S is functionally active and the complexed protein S is not active. Individuals congenitally deficient in protein S ae subject to recurrent thromboembolicevents. At least two classes of protin S deficiency occur.Some patienshavedecreased levels of protein S antigen and reduced protein S functional activity. A second group of deficient individuals have normal levels of protein S antigen but most or all their protein S is complexed to C4b-binding protein and they have little or no functional protein S activity. Such a protein S distribution could result from abnormal forms of protein S or C4b-binding protein or some other abnormal plasma or cellular component. Patients with functionally inactive forms of protein S have yet to be identified. Identification of protein S deficient individuals is complicated by thepossible effect of sex hormones on plasma protein S levels. Total protein S antigen is reduced during pregnancyand during oral contraceptive administration. This finding is of practicalclinical importance since the decrease in protein S which occurs during pregnancy may be an added risk factor for congenitally protein S deficient women and may explain why some proteinS deficient women experience their first episode of thrombosis during pregnancy.In addition to having anticoagulant properties, activated protein C enhances fibrinolysis, at least in part,by inhibiting the inhibitor of tissueplasminogen activator. This profibrinolytic effect is enhanced by protein S and cell surfaces. This protection of plasminogen activator activity suggests that the combination of tissue plasminogen activator and activated protein C may be useful in the treatment of coronary artery thrombi. Tissueplasminogen activator would promote clot lysis while activated protein C protected the plasminogen activatorfrom inhibition and also prevented further clot deposition. There is no evidence at present that fibrinolytic activity is reduced in protein C deficient individuals. The possible clinical relevance of this aspect of protein Cfunction in the predisposition of protein C deficient individuals to thrombosis remains to be defined.
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Wachtfogel, Yanina T., Yizhar Floman, Meir Liebergall, Robert W. Colman i Amiram Eldor. "PLATELET ALPHA2-ADRENERGIC RECEPTOR ABNORMALITIES IN PATIENTS WITH IDIOPATHK: SCOLIOSIS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644567.

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Idiopathic scoliosis is a genetic multisystem disease involving skeletal, biochemical, central nervous svstem, muscle and blood platelet abnormalities. Platelets of patients with idiopathic scoliosis have been shown to have decreased adenosine diphosphate and epinephrine-induced aggregation. Similarities between the contractile protein system of platelets and muscle have made the platelet a popular model for certain aspects of muscle physiology. This study confirmed that 64% of the patient platelets tested exhibited a significantly decreased sensitivity to aggregation bv epinephrine. In seven of the eleven patients studied, epinephrine induced aggregation was markedly decreased, i.e., the threshold of agonist was markedly elevated ≥11 uM). The geometric mean concentration of epinephrine required to produce complete second-wave aggregation in idiopathic scoliosis patients was 8μM. as compared to a control concentration of luM. We therefore examined the platelet alpha2-adrenergic receptors of 17 patients with idiopathic scoliosis bv measuring ligand binding using the selective antagonist, methyl yohimbine. Platelets from healthv individuals had 185 ± 16 sites per platelet with a Kd of 1.90 ± 0.32 nM, while patients with idiopathic scoliosis had 54 ± 22 sites per platelet with a of 1.02 ± 0.03 nM. The number of binding sites per platelet in idiopathic scoliosis patients were significantly decreased (p < 0.05) as compared to controls , while the was not significantly different (p > 0.05) between the two groups. Seven of these patients exhibited a significant decrease (p < 0.05) in the number of alpha2-adrenergic receptors on their platelets while the binding in 7 additional patients was undetectable.Three patients exhibited normal receptor number and affinity as compared to normal individuals. This study indicates a profound alteration in the number and function of the alpha2-adrenergic receptors in platelets of patients with idiopathic scoliosis and indicates the functional heterogeneity of the receptor disorder. Further investigation of platelet abnormalities may give insight into the putative muscle defects.
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Tran, Phat L., Jessica R. Gamboa, Katherine E. McCracken, Jeong-Yeol Yoon i Marvin J. Slepian. "Interaction With Nanoscale Topography: The Use of Nanowell-Trapped Charged Ligand-Bearing Nanoparticle Surfaces To Modulate Physiological Focal Adhesions in Endothelial Cells". W ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93345.

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Achieving cell adhesion, growth and homeostasis on an underlying biomaterial surface may be a desirable feature in implant device design and tissue engineering. Insight has been gained from numerous cell patterning strategies where spatial cues and physical constraints have been shown to regulate the structure and function of cells. Despite significant advances in modifying substrates for cellular attachment, migration and proliferation, the achievement of confluent and aligned growth of functional endothelial cells on cardiovascular blood-contacting implants under physiologically significant wall shear stress has proven difficult. Recently we have reported on a method that enhances cellular adhesion under flow conditions on synthetic polymer surfaces, without reliance on pro-adhesive protein biomaterials, which are often thrombogenic. In this method we utilize electron beam lithography and size-dependent self-assembly to fabricate line arrays of nanowells allowing entrapment and retention of charged nanoparticles, covalently conjugated with a RGD adhesive ligand, GRGDSPK. This approach is an additive strategy of combining substrata topographic alteration, electrostatic charge and biochemical ligands, all uniquely incorporated as an ensemble of charged, ligand-bearing nanoparticles entrapped in arrays of nanowells. However, the modulation of endothelial cell physiologic mechanisms as a result of ensemble surface exposure remains to be characterized. In this report, we extend our studies and probe cell physiologic mechanisms altered as a result of nanofeatured surface exposure. We first examined the functional intactness or normalcy of endothelial cells adherent to the nanofeatured ensemble surface utilizing standard immunostaining and flow cytometry methods. We found β1-integrin expression dominated quiescent adherent endothelial cells while αVβ3-integrins expression was more common in migratory cells. Endothelial cells were noted to express high levels of PECAM-1 over time when exposed to nanofeatured surface and RGD peptides. For understanding the contribution of the nanofeatured surface (entrapped RGD conjugated nanoparticles) to cell adhesion, cytochalasin B was used to alter cell spreading. Confocal microscopy illustrated the uptake of nanoparticles in endothelial cells on composite surfaces, as well as the inhibition of this endocytosis by cytochalasin B. After prohibiting the cells from engulfing nanoparticles, we found an 80% reduction in cell adhesion; suggesting that an endocytic mechanism might play a role in maintaining cell adhesion. Nanofeatured ensemble surfaces appear to be good substrates for achieving a high level of EC adhesion, with maintained growth and stability.
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