Relevant bibliographies by topics / Cellular effect

Academic literature on the topic 'Cellular effect'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Cellular effect"

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Naphade, Vaishali D., Gaurav Parihar, D. K. Jain, and Atul R. Bendale. "Investigation of the effect of agomelatine on cellular and humoral immunity in mice." Bulletin of the Karaganda University. “Biology, medicine, geography Series” 104, no. 4 (December 30, 2021): 97–103. http://dx.doi.org/10.31489/2021bmg4/97-103.

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Agomelatine has primarily been described as an antidepressant drug for laborartory animals. In the present study, agomelatine showed an overall stimulatory effect on the specific, as well as on non-specific immune functions of mice. Stimulatory effects were observed at 25 mg/kg. Administration of agomelatine in human beings is simple as it is available in the dosage form. The general immunomodulatory effects of agomelatine need further investigation for its use in the cases of clinical immunostimulation and in order to understand the precise mechanism of action for the stimulatory effect of the drug. The present result suggests that agomelatine may stimulate both the cellular and humoral immunity. Effects were evaluated at different doses of 1, 5 and 25 mg/kg using various parameters such as effect on hematological parameters. The results were further utilized to evaluate the activity on the cellular and humoral branches of immunity.
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Goldstein, Dora B. "Effect of alcohol on cellular membranes." Annals of Emergency Medicine 15, no. 9 (September 1986): 1013–18. http://dx.doi.org/10.1016/s0196-0644(86)80120-2.

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Goldstein, Dora B. "Effect of ethanol on cellular membranes." Annals of Emergency Medicine 15, no. 1 (January 1986): 91. http://dx.doi.org/10.1016/s0196-0644(86)80499-1.

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Wu, Miaozong, Jacqueline Fannin, Kevin M. Rice, Bin Wang, and Eric R. Blough. "Effect of aging on cellular mechanotransduction." Ageing Research Reviews 10, no. 1 (January 2011): 1–15. http://dx.doi.org/10.1016/j.arr.2009.11.002.

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Sharma, Dr K. Krishna, Dr Udaya Kumara K, Dr Thirumaleshwara Prasada H, and Sriharisukesh N. Sriharisukesh N. "Effect of Yoga Therapy on Cellular Rejuvenation and Improvement of Concentration (A Pilot Study." Indian Journal of Applied Research 4, no. 8 (October 1, 2011): 657–61. http://dx.doi.org/10.15373/2249555x/august2014/172.

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Kim, Hyun Young, Bo Ra Hwang, Ting Ting Wu, and Eun Ju Cho. "The protective effect of Perilla frutescens from ONOO--induced oxidative stress and antiaging effect under cellular system." Korean Journal of Agricultural Science 39, no. 4 (December 31, 2012): 467–71. http://dx.doi.org/10.7744/cnujas.2012.39.4.467.

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Sirolli, V., E. Ballone, S. Di Stante, L. Amoroso, and M. Bonomini. "Cell Activation and Cellular-Cellular Interactions during Hemodialysis: Effect of Dialyzer Membrane." International Journal of Artificial Organs 25, no. 6 (June 2002): 529–37. http://dx.doi.org/10.1177/039139880202500607.

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During hemodialysis (HD), circulating blood cells can be activated and also engage in dynamic interplay. These phenomena may be important factors behind dialysis membrane bio(in)compatibility. In the present prospective cross-over study, we have used flow cytometry to evaluate the influence of different dialysis membranes on the activation of circulating blood cells (leukocytes, platelets) and their dynamic interactions (formation of circulating platelet-leukocyte and platelet-erythrocyte aggregates) during in vivo HD. Each patient (n = 10) was treated with dialyzers containing membranes of cellulose diacetate, polysulfone and ethylenevinylalcohol (EVAL) in a randomized order. Upregulation of adhesion receptor expression (CD15s, CD11b/CD18) occurred mainly with the cellulosic membrane, though an increase in CD11b/CD18 circulating on neutrophils was also found with both synthetic membranes. Circulating activated platelets (P-selectin/CD63-positive platelets) increased during HD sessions with cellulose diacetate and polysulfone. An increased formation of platelet-neutrophil aggregates was found at 15 and 30 min during dialysis with cellulose diacetate and polysulfone but not with EVAL. Platelet-erythrocyte aggregates also increased with cellulose diacetate and at 15 min with polysulfone as well. Generally in concomitance with the increase in platelet-neutrophil coaggregates, there was an increased hydrogen peroxide production by neutrophils. The results of this study indicate that cellular mechanisms can be activated during HD largely depending on the membrane material, EVAL causing less reactivity than the other two membranes. It appears that each dialysis membrane has multiple and different characteristics that may contribute to interactions with blood components. Our results also indicate that derivatizing cellulose (cellulose diacetate) may be a useful way to improve the biocompatibility of the cellulose polymer and that there may be great variability in the biocompatibility profile of synthetic membranes, dialysis with polysulfone being in general associated with a higher degree of cell activation than EVAL membrane.
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Schäfer, Julia, Lukas Welti, Anja Seckinger, Jürgen Burhenne, Dirk Theile, and Johanna Weiss. "Cellular effect and efficacy of carfilzomib depends on cellular net concentration gradient." Cancer Chemotherapy and Pharmacology 80, no. 1 (May 12, 2017): 71–79. http://dx.doi.org/10.1007/s00280-017-3335-4.

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Nakabayashi, Seiichiro, Kiyoshi Inokuma, and Antonis Karantonis. "Magnetic effect for electrochemically driven cellular convection." Physical Review E 59, no. 6 (June 1, 1999): 6599–608. http://dx.doi.org/10.1103/physreve.59.6599.

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Sandovsky-Losica, H., I. Berdicevsky, I. Tsarfaty, and E. Segal. "Effect ofCandida albicansmetabolite(s) on cellular actin." FEMS Microbiology Letters 215, no. 1 (September 2002): 57–62. http://dx.doi.org/10.1111/j.1574-6968.2002.tb11370.x.

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Dissertations / Theses on the topic "Cellular effect"

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Smit, B. S. "Cellular radiotoxicity of iodine-123." Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51646.

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Thesis (MSc)--University of Stellenbosch, 2000.
ENGLISH ABSTRACT: The Auger electron emitter iodine-123 was examined in the form of 4- [12311iodoantipyrineand as [12311Nal for its effectiveness in killing cells of different sensitivity to photon irradiation. Micronucleus assays showed that 4- [12311iodoantipyrineis two to three times more effective in cell inactivation than C2311Nai.This can be attributed to the fact that antipyrine, for reason of its lipid solubility, can enter cells and can reach the cell nucleus, whereas C231]Nai is excluded from the cytoplasm. The differential targeting of intra- and extracellular compartments was confirmed by radionuclide uptake experiments. In the nucleus, Auger decay conceivably is located on the DNA where it may invoke high-LET irradiation damage. Irradiation damage by [12311Naisl by long range y-irradiation and hence low-LET. Results of the present study demonstrate however that the enhancement of MN-frequency seen with 4-[123I]iodoantipyrine over [12311Nalis similar for all cell lines and that the narrowing of MN-response expected for 4- [12311iodoantipyrinedoes not occur. Experiments with the free radical scavenger, DMSO, indicated nearly identical dose reduction factors for both iodine-123 carriers. These two observations strongly suggest that the cell inactivation by 4- [12311iodoantipyrine is not by high-LET direct ionisation of DNA, but due to an indirect effect. The indirect radiation effect of Auger decay in the nucleus is attributed to shielding of DNA by histones. Such a protection mechanism is not unrealistic if it is realised that histones and DNA associate in a 1: 1 weight ratio and that higher order folding of the nucleosome chain into solenoids, loops, and chromatids generates considerable protein density. In the nucleosome core, the histone acta mer measures 7 nm and closely approximates the 10 nm dimention of the Auger electron range. It is suggested that the interlacing of protein density with DNA density suppresses direct ionisation from Auger decay at the DNA and directs the majority of Auger decay to the histones.
AFRIKAANSE OPSOMMING: Die Auger-elektron-uitstraler, jodium-123, is ondersoek in die vorm van 4- [123l]jodoantipirien en [12311Nal om die effektiwiteit te bepaal waarmee dit selle met verskillende grade van sensitiwiteit vir fotonbestraling doodmaak. Mikrokerntellings toon aan dat 4-[123I]jodoantipirien selle twee tot drie maal meer effektief inaktiveer as [12311Nal.Dit kan toegeskryf word aan die feit dat antipirien, as gevolg van sy vetoplosbaarheidseienskappe, die selle kan binnedring en die kern bereik, teenoor [12311Nalwat uitgesluit word uit die sitoplasma. Die differensiële blootstelling van intra- en ekstrasellulere gebiede is bevestig deur radionukliedopname eksperimente. In die selkern vind Auger verval waarskynlik by die DNA plaas waar dit hoë-LET stralingskade veroorsaak. Stralingskade afkomstig van [1231]Nalis deur langafstand y-strale en dus lae-LET. Die resultate van die huidige studie bewys egter dat die verhoogde mikrokernfrekwensie van 4-[12311jodoantipirienteenoor [1231]Nal dieselfde is vir al die sellyne en dat die vernouïng van mikrokernreaksie soos verwag met 4- [12311jodoantipirien, nie plaasvind nie. Eksperimente met die vryradikaalopruimer, DMSO, dui op feitlik identiese dosis-modifiseringsfaktore vir beide jodium-123 draers. Hierdie twee waarnemings is 'n besliste aanduiding dat die selinaktivering deur 4-[12311jodoantipiriennie deur hoë-LET direkte ionisering van DNA plaasvind nie, maar eerder deur indirekte stralingsaksie. Die indirekte stralingseffek van Augerverval in die kern kan toegeskryf word aan afskerming van DNA deur histone. So 'n beskermingsmeganisme is nie onrealisties nie, as in ag geneem word dat histone en DNA in 'n 1: 1 gewigsverhouding assosieer en dat hoër orde vouïng van die nukleosoomketting tot solenoïede, lusse en chromatiede 'n beduidende protïendigtheid genereer. In die nukleosoomkern is die histoon-oktameer ongeveer 7 nm in deursnit en dus vergelykbaar met die 10 nm reikafstand van die Auger elektrone. Dit word voorgestel dat die ineengeweefdheid van die protien-digtheid met die DNA-digtheid die direkte ionisering van die DNA tydens Auger verval onderdruk en dat die meeste van die Auger verval in die histone plaasvind.
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Muhamad, Nur Airina. "Cellular basis of magnetic sensation." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610344.

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Willcocks, James Peter. "Magnesium in cellular energetics." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:f4f5de76-8c72-4b42-8bd4-eb151485d47e.

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Most cellular magnesium is bound, yet it is the concentration of free magnesium, [Mg2+]free, in red blood cells that is vital in the regulation of enzyme activity and ion transport. It is unknown how changes in total blood magnesium affect the [Mg2+]free within red blood cells or in tissue, because the presence of other cations, especially H+ and potassium, K+ , affects the degree to which Mg2+ is bound. Consequently, this Thesis presents a new 31P NMR spectroscopic method to measure [Mg2+]free in blood, which analyses the changes in the phosphorus chemical shifts of ATP and 2,3-DPG using theoretical equations expressing the observed chemical shift as a function of pH, K+ and [Mg2+]free, over the pH range of 5.75 to 8.5 and [Mg2+]free range 0 to 5 mM. The equations were adjusted for the binding of haemoglobin to ATP and DPG, which required knowledge of the intracellular concentrations of ATP, DPG, K+ and Hb. These equations enabled, for the first time, the simultaneous analyses of the chemical shifts of 3P-DPG and β-ATP to measure both intracellular 04- pH and [Mg2+]free in normal and sickle blood. To simulate in vivo 100% oxygenated blood, samples were prepared for analysis by equilibration with a mixture of O2 and CO2, adjusted to give a pCO2 of 40 mmHg and pO2 > 150 mmHg. Under these conditions, normal whole blood had an intracellular pH of 7.20 ± 0.02 and a [Mg2+]free of 0.41 ± 0.03 mM (n = 33). Further work determined blood pH and [Mg2+]free for several clinical conditions including sickle cell anaemia, pre-eclampsia, hypoxia, patients with sub-arachnoid haemorrhage and chronic fatigue syndrome. This Thesis has demonstrated the potential of this new technique to evaluate the importance of [Mg2+]free in the regulation of metabolite concentration and metabolic function, and to elucidate some of the properties of magnesium transport across the erythrocyte cell membrane.
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Hashimoto, Kyoichi. "Cellular context-dependent consequences of Apc mutations on gene regulation and cellular behavior." Kyoto University, 2018. http://hdl.handle.net/2433/230974.

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Khan, Abrar Ul Haq. "Cellular Metabolism Regulates Anti-Oxidant Response Through ERK5-MEF2 Pathway." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT036/document.

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Le métabolisme cellulaire est la source principale d’énergie et les cellules cancéreuses ont un métabolisme différent des cellules non transformées. La cellule tumorale a tendance à éviter l’activité mitochondriale et ainsi la phosphorylation oxydative, pour lui préférer la voie de la glycolyse pour la production d’énergie (Effet Warburg). Cette altération du métabolisme est si bénéfique pour les cellules en croissance que cela favorise la croissance tumorale et supprime la réponse immunitaire anticancéreuse. La spécificité de ce métabolisme en fait une cible intéressante pour le développement de thérapies anticancéreuses. Mon travail de thèse comporte deux parties. La première partie décrit que lorsque les cellules cancéreuses sont forcées à utiliser la voie mitochondriale comme source d’énergie à travers l’oxydation phosphorylative, elles initient un mécanisme antioxydant pour tolérer les effets délétères des espèces oxygénées réactives (EOR ou ROS pour reactive oxygene species) produites au cours de l’activité mitochondriale. La stimulation mitochondriale entraîne l’activation de la voie de signalisation ERK5-MEF2, et cette dernière engendre un mécanisme antioxydant de deux façons.Initialement, nous avons observé que MEF2 régule positivement l’expression de miR23a, et ce dernier inhibe l’expression de KEAP1. Cette protéine est responsable de la dégradation ubiquitine dépendante de NRF2, un régulateur clé de la réponse antioxydante cellulaire. L’inhibition de KEAP1 empêche la dégradation cytoplasmique de NRF2. Consécutivement à cela la concentration cytoplasmique en NRF2 augmente ce qui engendre sa translocation dans le noyau où il se lie à une séquence élément de réponse antioxydant (ARE) dans la région promotrice de nombreux gènes antioxydants, initiant ainsi leur transcription. Plus tard nous avons observé que l’activation de la voie ERK5-MEF2 induisait directement la synthèse de novo de NRF2, induisant sa translocation nucléaire et un mécanisme antioxydant. L’inhibition de la voie ERK5-MEF2 altère la réponse antioxydante, sensibilisant ainsi les cellules au stress oxydant.La seconde partie de mon travail a exploré les mécanismes à l’origine des effets hypolipémiants du dichloroacétate (DCA). Le DCA est une petite molécule qui inhibe la PDK1 et permet au pyruvate d’entrer dans la mitochondrie. Il a été utilisé en clinique dans le passé pour baisser les taux plasmatiques de cholestérol mais le mécanisme n’était pas clair et nous l’avons décris. Le DCA force les cellules à entrer en oxydation phosphorylative ce qui active la voie ERK5-MEF2. Cette voie augmente directement l’expression du LDLR (Low Density Lipoprotein Receptor ; récepteur aux lipoprotéines de basse densité) qui permet l’endocytose des LDL riches en cholestérol qui sont responsables de la plupart des maladies cardiovasculaires. L’inhibition de cette voie supprime l’afflux de lipides et par conséquent serait une cible intéressante pour de futures recherches puisque de hauts taux de cholestérols sont directement corrélés avec une augmentation du risque d’athérosclérose et de toutes les complications mortelles qu’il entraine.Notre prochain objectif est d’explorer les autres mécanismes cellulaires régulés par la voie ERK5-MEF2. Sur la base de nos résultats préliminaires, nous proposons que cette voie non seulement régule l’expression du LDLR mais aussi celle de nombreux autres gènes qui sont impliqués directement ou indirectement dans le métabolisme des lipides
Cellular metabolism is the main source of energy and cancer cells has different metabolism than non-transformed cells. Tumor cell tends to avoid mitochondrial activity and oxidative phosphorylation (OXPHOS) and prefer glycolysis for energy production (Warburg effect). This alteration in metabolism is beneficial for growing cells in many ways that promote tumor growth and suppress the anti-cancer immune response. This specific metabolism is an auspicious target for the better development of cancers chemotherapies.My thesis work comprises two parts. The first portion describes that when cancer cells are forced to utilize their mitochondria in order to obtain the energy from OXPHOS they initiate an antioxidant mechanism to cope with the deleterious effects of reactive oxygen species (ROS) produced during mitochondrial activity. Mitochondrial stimulation leads to activation of ERK5-MEF2 signaling pathway, which triggers the antioxidant mechanism by at least two ways.Initially we observed that MEF2 up regulates the expression of miR23a, which inhibits KEAP1 expression. This protein is responsible for ubiquitinational degradation of NRF2, a master regulator of the antioxidant response in cells. The inhibition of KEAP1 prevents the NRF2 cytoplasmic degradation. This results in high built up of NRF2 in cytoplasm that translocates to nucleus where it binds to ARE (antioxidant response element) in the upstream promoter region of many antioxidant genes hence initiates their transcription. Latter we observed that activation of ERK5-MEF2 pathway directly results in de novo synthesis of NRF2, resulting in nuclear translocation and triggering of the antioxidative mechanism. Inhibition of ERK5-MEF2 pathway impairs the cellular antioxidant response, thus sensitizing cells towards oxidative stress.The second part of my work explored the mechanism behind the lipid lowering effects of dichloroacetate (DCA). DCA is a small molecule, which inhibits the PDK1 and enables pyruvate to enter the mitochondria. It was used clinically in past to lower the plasma cholesterol level but the underlying mechanism was not clear and we describe it here. DCA forces cells to perform OXPHOS, which activate the ERK5-MEF2 pathway. This pathway directly up-regulates the expression of Low Density Lipoprotein Receptors (LDLR) that are mainly involved in the endocytosis of cholesterol-rich low density lipoproteins, which are responsible for the majority of cardiovascular diseases. Inhibition of this pathway suppresses lipid influx and hence, it would be an interesting target of future investigation since high cholesterol level is the main cause of various life threatening diseases and the development of atherosclerosis.Our next goal is to exploit other possible cellular mechanism regulated by ERK5-MEF2 pathway. Based on our preliminary data, we propose that this pathway not only regulate the LDLR expression but many other genes, which are directly or indirectly involved in lipid metabolism
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Broderick, Peter. "The effect of EBV on host cellular gene expression." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444349.

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Chakravarthy, Usha. "The effect of gamma radiation on intraocular cellular proliferation." Thesis, Queen's University Belfast, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317046.

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Oyman, Sena. "Cellular integrity : its effect on in-vitro starch digestion." Thesis, University of Nottingham, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440288.

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Chu, Yu-Hsuan. "Custom Fluorophores for Investigating the Cellular Uptake Mechanisms and Side-Effects of Pharmaceuticals." PDXScholar, 2015. http://pdxscholar.library.pdx.edu/open_access_etds/2343.

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There is a significant current need to elucidate the molecular mechanisms of the side-effects caused by widely-used pharmaceuticals. Examples include the acute nephrotoxicity and irreversible ototoxicity promoted by the cationic drugs gentamicin and cisplatin. Gentamicin is an aminoglycoside antibiotic used for the prevention and treatment of life-threatening gram-negative bacterial infections, such as tuberculosis and meningitis. Cisplatin is used to treat a broad spectrum of cancers including head and neck, ovarian, cervical, stomach, bladder, sarcoma, lymphoma, testicular cancer and others. The objective of this study is to design and synthesize rhodamine derivatives that can be used for the construction of geometrically well-defined cationic drug conjugates. The long-term goal is to use the conjugates as tools to aid in elucidating the properties and identities of ion channels involved in the uptake of cationic pharmaceuticals into kidney and cochlear hair cells. This will shed light on the origin and potential prevention of unwanted side effects such as nephrotoxicity and ototoxicity associated with specific cationic drugs. A series of extended rhodamine analogs with reactive groups for biomolecule conjugation has been synthesized. These fluorophores show similar spectral properties to their prototype, Texas Red succinimidyl ester (TR-SE). However, they contain rigid linkers between the fluorophore and amine-reactive moiety. The resultant gentamicin conjugates of these materials are rigidified enabling one to assess channel pore dimensions without the confounding issue of conjugate folding. Preliminary cell studies are promising, as one observes reduced gentamicin uptake in both kidney and sensory hair cell upon systematically increasing the dimension of the fluorophore. This work has enabled us to tentatively assign the maximum dilated MET channel pore size as between 1.44 nm to 1.56 nm. However, this preliminary finding, though encouraging, needs further validation via ongoing studies with larger diameter fluorophore conjugates, A cisplatin-Texas Red conjugate has also been synthesized to enable studies of cellular uptake mechanisms. This conjugate preserves not only the spectral properties of Texas Red after conjugation, but also the cytotoxicity of cisplatin. This has been validated in zebrafish. The series of rhodamine probes that have been conjugated to gentamicin should be similarly useful for cisplatin studies. These studies are planned. Additional future work includes the synthesis of semi-flexible (glycol) and flexible (alkyl) linkers to evaluate structure-activity relationships.
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Hendrichsen, Melissa K. "Thermal effect and fault tolerance in quantum dot cellular automata." Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1314329.

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To have a useful QCA device it is first necessary to study how to control data flow in a device, then study how temperature and manufacturing defects will affect the proper output of the device. Theoretically a "quantum wire" of perfectly aligned QCA cells at zero Kelvin temperature has been examined. However, QCA processors will not be operating at a temperature of zero Kelvin and inherently the manufacturing process will introduce defects into the system. Many different types of defects could occur at the device level and the individual cell level, both kinds of defects should be examined. Device defects include but are not limited to linear and/or rotational translation, and missing or extra cell(s). The internal cell defects would include an odd sized cell, and one or more miss-sized or dislocated quantum dot(s). These defects may have little effect on the operation of the QCA device, or could cause a complete failure. In addition, the thermal effect on the QCA devices may also cause a failure of the device or system. The defect and thermal operating limit of a QCA device must be determined.In the present investigation, the thermal and defect tolerance of clocked QCA devices will be studied. In order to study tolerance of QCA devices theoretical models will be developed. In particular, some existing computer simulation programs will be studied and expanded.
Department of Physics and Astronomy
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Books on the topic "Cellular effect"

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H, Roth Sheldon, Miller Keith W, and International Conference on Molecular and Cellular Mechanisms of Anesthesia (3rd : 1984 : University of Calgary), eds. Molecular and cellular mechanisms of anesthetics. New York: Plenum Medical Book Co., 1986.

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H, Roth Sheldon, and Miller Keith W, eds. Molecular and cellular mechanisms of anesthetics. New York: Plenum Medical, 1986.

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J, Berry L., ed. Cellular biology of endotoxin. Amsterdam: Elsevier, 1985.

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S, Wonnacott, Russell M. A. H, and Stolerman Ian P, eds. Nicotine psychopharmacology: Molecular, cellular, and behavioural aspects. Oxford [England]: Oxford University Press, 1990.

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Wilson, J. W. Cellular repair/misrepair track model. [Washington, DC]: National Aeronautics and Space Administration, Office of Management, Scientific and Technical Information Program, 1991.

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Edward, Bittar E., and Bittar Neville, eds. Molecular and cellular pharmacology. Greenwich, Conn: JAI Press, 1997.

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1945-, Fukuda Minoru, and Hindsgaul Ole, eds. Molecular and cellular glycobiology. Oxford: Oxford University Press, 2000.

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W, Cowley Allen, Liard Jean-Francois, Ausiello D. A, and International Vasopressin Conference (2nd : 1987 : Smugglers Notch, Vt.), eds. Vasopressin: Cellular and integrative functions. New York: Raven Press, 1988.

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Rüegg, Johann Caspar. Calcium in muscle contraction: Cellular andmolecular physiology. 2nd ed. Berlin: Springer-Verlag, 1992.

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Steve, Schaffer, Lonbardini J. Barry, Huxtable Ryan J, and International Taurine Symposium '97: Cellular and Regulatory Mechanisms (1997 : Tucson, Ariz.), eds. Taurine 3: Cellular and regulatory mechanisms. New York: Plenum Press, 1998.

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Book chapters on the topic "Cellular effect"

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Rahman, Safikur, Jihyun Park, and Jihoe Kim. "Osmolytes Offset the Urea’s Effect on Protein Structure and Function." In Cellular Osmolytes, 77–96. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3707-8_4.

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Bhatia, Saloni, Sharda Vashisth, and Ashok Salhan. "Cellular Radiations Effect on Human Health." In Proceedings of First International Conference on Information and Communication Technology for Intelligent Systems: Volume 1, 213–19. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30933-0_23.

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Jahan, Fahmida, and Jeffrey T. Wigle. "Diverse Cellular Origins of Cardiac Fibroblasts." In Cardiac Fibrosis and Heart Failure: Cause or Effect?, 125–45. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17437-2_8.

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Swales, J. D. "Vascular Smooth Muscle Cell in Hypertension: Dissecting Out Cause and Effect." In Cellular Aspects of Hypertension, 13–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-00983-3_2.

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Makino, Naoki, Hirosuke Matsui, Kazuhiro Masutomo, Tomoji Hata, and Takashi Yanaga. "Effect of Angiotensin Coverting Enzyme Inhibitor on Regression in Cardiac Hypertrophy." In Cellular Function and Metabolism, 23–28. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7_4.

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Zhang, Huidong. "Effect of Environmental Carcinogens on Cellular Physiology." In DNA Replication - Damage from Environmental Carcinogens, 27–34. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7212-9_5.

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Virág, László, Tetsushi Furukawa, and Masayasu Hiraoka. "Modulation of the Effect of Glibenclamide on KATP Channels by ATP and ADP." In Cellular Function and Metabolism, 209–15. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7_28.

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Saxena, Ajit Kumar, and Amit Kumar. "Effect of Cyclophosphamide on Chromosomes." In Fish Analysis for Drug and Chemicals Mediated Cellular Toxicity, 7–24. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-4700-3_2.

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Mesaeli, Nasrin, and Vincenzo Panagia. "Effect of membrane modifiers on polyphosphoinositide synthesis in rat heart sarcolemma." In Cellular Regulation by Protein Phosphorylation, 483–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75142-4_61.

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Jobst, Kass A., Alexander Klenov, Kira C. M. Neller, and Katalin A. Hudak. "Effect of Depurination on Cellular and Viral RNA." In Modified Nucleic Acids in Biology and Medicine, 273–97. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34175-0_12.

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Conference papers on the topic "Cellular effect"

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"The Effect of Allicin on ZNF703 Gene Expression in GCC Lines." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916405.

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"The Effect of Inorganic Mercury Intoxication on Heart Myofibrils in Rats." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916431.

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"The Effect of Hydroalcoholic Extract of Junipers communis on Proliferation BHK Cells." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916411.

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Haridim, Motti, Boris Levin, Stav Revich, Stefan Chulski, and Ronan Sauleau. "Effect of head heterogeneity on a cellular phone field." In 2013 IEEE International Symposium on Electromagnetic Compatibility - EMC 2013. IEEE, 2013. http://dx.doi.org/10.1109/isemc.2013.6670401.

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Qian, Xu, He Hujun, Yang Guangtao, and Yang Xu. "Effect of Formaldehyde on Cellular Proliferation of HEK293 Cells." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.122.

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Nath, N. P., S. R. Parija, P. K. Sahu, and S. S. Singh. "Effect of dynamic profile based paging in cellular network." In 2015 Annual IEEE India Conference (INDICON). IEEE, 2015. http://dx.doi.org/10.1109/indicon.2015.7443590.

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Alkhader, Maen, and Murat Vural. "Influence of Cellular Topology on Dynamic Response of Solid Foams." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15638.

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Current processing techniques enable the manufacture of cellular cores to prescribed cell sizes and densities. Moreover, the rapid advance in additive manufacturing techniques promises that, in the near future, the fabrication of functional cellular structures will be achieved with desired cellular topologies tailored to specific application in mind. In this perspective, it is essential to develop a detailed understanding of the relationship between mechanical response and topology in cellular structures. The present work reports the initial results of a computational investigation in this direction. The fundamental issues addressed in the present study are (i) generation of stochastic cellular structures by using Voronoi tessellations, (ii) quantitative measure of cellular topology, (iii) uniqueness of mechanical response, (iv) specimen size effect, (v) boundary effect, and (vi) high-strain-rate effects.
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Li, Weide, and Xiaohu Guo. "A Cellular Automaton Model for Two Competitive Populations with Allee Effect and Overcrowding Effect." In 2011 International Conference on Computer and Management (CAMAN). IEEE, 2011. http://dx.doi.org/10.1109/caman.2011.5778752.

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Sarvestani, Alireza. "A Theoretical Analysis for the Effect of Substrate Elasticity on Cellular Adhesion." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13311.

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Cell behavior is mediated by variety of physiochemical properties of extracellular matrix (ECM). Material composition, surface chemistry, roughness, and distribution pattern of cell adhesive proteins are among the ECM properties which are known to modulate various cellular physiological functions. Mechanical stiffness of ECM in particular is found to be a major regulator for multiple aspects of cellular function. Experiments show that cells in general, exhibit an apparent adhesion preference for stiffer substrates with a larger projected spread area with increasing the substrate stiffness. In addition, it seems that the effect of substrates elasticity is strongly coupled with adhesivity of the substrate; on relatively stiff substrates the spread area of the cells exhibits strong biphasic dependence to the changes in ligand density, whereas on soft substrates their limited spreading is much less sensitive to the density of surface ligands. This study aims to propose a theoretical basis for the interplay between substrate elasticity and cellular adhesion, using an equilibrium thermodynamic model. Within this framework, the equilibrium contact area is assumed to ensure minimization of the free energy contributed by interfacial adhesive and repulsive interactions between the membrane and substrate as well as the deformation of cell and substrate. Hence, this thermodynamic model overlooks the contribution of intracellular signaling or actively regulated cytoskeleton and assumes that cell adhesion is solely a result of the balance between the membrane-substrate repulsive potentials, stored elastic energy, binding enthalpy, and mixing entropy of mobile receptors. The predictions of this purely mechanistic model for cell adhesion qualitatively follow the experimental results featuring the variation of cell spread area on compliant bio-adhesive substrates. This suggests that the mechanistic pathways inherent to membrane-substrate interactions may be equally important as intracellular signaling pathways to mediate the cellular adhesion.
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Ajdari, Amin, Hamid Nayeb-Hashemi, and Paul K. Canavan. "Effect of Defect on Elastic-Plastic and Creep Behavior of Cellular Materials." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42056.

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Cellular solids, such as foams, are widely used in engineering applications. In these applications, it is important to know their mechanical properties and the variation of these properties with the presence of defects. Several models have been proposed to obtain the mechanical properties of cellular materials. However, some of these models are based on idealized unit cell structures, and are not suitable for finding the mechanical properties of cellular materials with defects. Furthermore, the creep response changes in cellular solids when the exposed temperature is higher than 1/3 of the material’s melting temperature. The objective of this work is to understand the effect of missing walls and filled cells on mechanical and creep behavior of both the regular hexagonal and non-periodic Voronoi structures using finite element analysis. The finite element analysis showed that on average the non periodic structures have inferior mechanical properties compared to that of the regular hexagonal structures with the same relative density. The yield stress of Voronoi structures had a mean of 27% lower compared to that of the hexagonal structure with the same relative densities. Defects, introduced by removing cell walls at random locations, caused a sharp decrease in the effective mechanical properties of both Voronoi and periodic hexagonal honeycombs. However, our results indicated that elastic properties of Voronoi Structures are more sensitive to missing walls when compared to those of regular honeycomb structures. The yield strength of Voronoi and regular honeycombs exhibited the similar sensitivity to cell wall removal. For creep analysis, the results suggest that removal of struts dramatically increases the creep rate. In the case of filled cells, regular honeycomb structures showed less sensitivity to the defect compared to Voronoi structures. The overall elastic modulus of the structure increased by 11% when 5% of cells were filled in regular hexagonal honeycombs while for Voronoi structure it had more significant effect (22% increase). The results also show that filled cell did not have a significant effect on yield strength of the regular and Voronoi structures.
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Reports on the topic "Cellular effect"

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Chang-Liu, Chin-Mei, and G. E. Wolschak. Effect of passage number on cellular response DNA-damaging agents: cell survival and gene expression. Office of Scientific and Technical Information (OSTI), March 1996. http://dx.doi.org/10.2172/206623.

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Chang-Liu, C. M., and G. E. Woloschak. Effect of passage number on cellular response to DNA-damaging agents: Cell survival and gene expression. Office of Scientific and Technical Information (OSTI), August 1997. http://dx.doi.org/10.2172/515535.

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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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Andersen, Martin, Johanna Catherine Maclean, Michael Pesko, and Kosali Simon. Effect of a Federal Paid Sick Leave Mandate on Working and Staying at Home During the COVID-19 Pandemic: Evidence from Cellular Device Data. Cambridge, MA: National Bureau of Economic Research, May 2020. http://dx.doi.org/10.3386/w27138.

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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Lee, Luke P. Smart Gold Nanobowls (Nano-Crescent Moon) with Sub-10 nm Circular Edge for Local Electromagnetic Field Enhancement Effect, Spatial, and NIR Temporal/Thermal Modulations for Molecular and Cellular Dynamic Imaging. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada443279.

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Weaver, B. D. A Theory of Radiation Effects in Cellular Devices. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada454240.

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Merling, Randall K. HTLV-1 Tax Effects on Cellular Mitotic Regulation. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ad1014020.

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Wood, W. G. Mechanisms of Alcohol Induced Effects on Cellular Cholesterol Dynamics. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada398121.

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Wood, W. G. Mechanisms of Alcohol Induced Effects on Cellular Cholesterol Dynamics. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada431885.

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