Academic literature on the topic 'Calcium channel variance'
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Journal articles on the topic "Calcium channel variance"
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Sah, P. "Properties of channels mediating the apamin-insensitive afterhyperpolarization in vagal motoneurons." Journal of Neurophysiology 74, no. 4 (October 1, 1995): 1772–76. http://dx.doi.org/10.1152/jn.1995.74.4.1772.
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1. Whole cell recordings were obtained from neurons of the dorsal motor nucleus of the vagus in transverse slices of guinea pig medulla. From a holding potential of -40 mV, short depolarizing voltage steps activated two calcium-dependent potassium currents, Gk(Ca),1 and Gk(Ca),2. 2. Gk(Ca),1 was completely blocked by apamin (100 nM). Gk(Ca),2 was apamin insensitive, voltage independent, and reversed close to the potassium equilibrium potential. 3. Activation of Gk(Ca),2 was associated with an increase in current variance. The channels underlying the slow component were analyzed by stationary and nonstationary fluctuation analysis. Current variance was linearly related to mean current for small current amplitudes but clearly deviated from linearity near the peak of Gk(Ca),2. The predicted single channel conductance was 6.8 +/- 2.5 (SE) pS. Probability of channel opening rose to at most 0.68. The average number of available Gk(Ca),2 channels on vagal neurons was 4,437 +/- 591. 4. Power spectra were constructed from the peak current. Spectra were well fitted with a single Lorentzian with a corner frequency of 72 +/- 7 Hz. The mean burst duration of the channels was 3.8 +/- 0.5 ms. These results indicate that a new type of calcium-activated channel underlies Gk(Ca),2.
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Meir, A., and R. Rahamimoff. "A voltage-dependent and calcium-permeable ion channel in fused presynaptic terminals of Torpedo." Journal of Neurophysiology 75, no. 5 (May 1, 1996): 1858–70. http://dx.doi.org/10.1152/jn.1996.75.5.1858.
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1. We used a preparation of fused presynaptic nerve terminals of Torpedo electromotor nerve and the patch-clamp technique for characterization of single ion channels. We report here of a large, nonselective ion channel which is highly voltage dependent. 2. The slope conductance of the I-V relation was estimated by either direct measurement of the single-channel current amplitude at different voltages (850 +/- 18 pS (SE); n = 9) or by variance analysis (834 +/- 23 pS; n = 5). 3. The voltage dependence was examined in three ways. At steady-state DC voltage conditions, NPo (the open probability times the number of channels in the patch) was estimated. At potentials < 0 mV, the probability of the channel to open is negligible and increases dramatically, within a very narrow voltage range, to > 50% at +8 mV (n = 8). 4. In pulse experiments, the activation time delay is shorter as the voltage step reaches more positive values. The mean time for half activation (T1/2) decreases from 15 ms at +10 mV to 4 ms at +30 mV (n = 5). 5. Ensemble currents exhibit rectification in response to voltage ramps at negative potentials (n = 10). 6. The channel was found to be nonselective. Its permeability to Na+, K+, Cl-, glutamate, Ba+2, and Ca+2, relative to Na+, was 1.00, 1.00, 1.22, 1.07, 0.85, and 0.62, respectively. 7. Based on the transport number of calcium, the calculated driving force, and the mean channel open time, we estimated the number of calcium ions entering the nerve terminal upon depolarization. This number is not substantially different from the number of ions entering through voltage-dependent, calcium-selective channels in other cells. 8. We speculate that this nonselective ion channel, may serve as a calcium entry route into the nerve terminal and hence be involved in transmitter release.
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Naumovic, Nada, Petar Slankamenac, Danka Filipovic, Vesna Ivetic, Snezana Tomasevic-Todorovic, and Ksenija Boskovic. "Effects of calcium antagonists on brain ischemia." Medical review 64, no. 5-6 (2011): 257–61. http://dx.doi.org/10.2298/mpns1106257n.
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Introduction. Stroke is the second leading cause of death in the world and the leading cause of serious, long term disability in adults; about half of those who survive become dependent on others in performing personal activities of daily living. Ischemia disturbs calcium cellular homeostasis, whereas calcium channel blockers re-establish it. This study was aimed at assessing benefits of calcium channel blockers on the outcome of rehabilitation of the patients afflicted by ischemic stroke. Material and Methods. The functional independence was measured by the Barthel index in 90 patients subjected to rehabilitative therapeutic treatment. The functional recovery of patients treated with calcium channel blockers and with other drugs (control) was compared and tested. Results. The analysis of variance (ANOVA) for the 0.5 confidence interval showed that the increases of the Barthel index values were significantly higher in the patients treated with calcium antagonists (p<0.5). Discussion. According to the literature, such an outcome is the result of improved brain blood f low auto-regulation, increased brain perfusion as well as of neuroprotective, antioxidative, platelet antiaggregatory effects of investigated drugs. Conclusion. The calcium channel blockers improved the outcome of rehabilitative therapeutic treatment significantly in the patients afflicted by ischemic stroke.
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Giannini, G., A. Conti, S. Mammarella, M. Scrobogna, and V. Sorrentino. "The ryanodine receptor/calcium channel genes are widely and differentially expressed in murine brain and peripheral tissues." Journal of Cell Biology 128, no. 5 (March 1, 1995): 893–904. http://dx.doi.org/10.1083/jcb.128.5.893.
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Ryanodine receptors (RyRs) are intracellular calcium release channels that participate in controlling cytosolic calcium levels. At variance with the probably ubiquitous inositol 1,4,5-trisphosphate-operated calcium channels (1,4,5-trisphosphate receptors), RyRs have been mainly regarded as the calcium release channels controlling skeletal and cardiac muscle contraction. Increasing evidence has recently suggested that RyRs may be more widely expressed, but this has never been extensively examined. Therefore, we cloned three cDNAs corresponding to murine RyR homologues to carry a comprehensive analysis of their expression in murine tissues. Here, we report that the three genes are expressed in almost all tissues analyzed, where tissue-specific patterns of expression were observed. In the uterus and vas deferens, expression of RyR3 was localized to the smooth muscle component of these organs. In the testis, expression of RyR1 and RyR3 was detected in germ cells. RyR mRNAs were also detected in in vitro-cultured cell lines. RyR1, RyR2, and RyR3 mRNA were detected in the cerebrum and in the cerebellum. In situ analysis revealed a cell type-specific pattern of expression in the different regions of the central nervous system. The differential expression of the three ryanodine receptor genes in the central nervous system was also confirmed using specific antibodies against the respective proteins. This widespread pattern of expression suggests that RyRs may participate in the regulation of intracellular calcium homeostasis in a range of cells wider than previously recognized.
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Prakriya, Murali, and Richard S. Lewis. "Regulation of CRAC Channel Activity by Recruitment of Silent Channels to a High Open-probability Gating Mode." Journal of General Physiology 128, no. 3 (August 28, 2006): 373–86. http://dx.doi.org/10.1085/jgp.200609588.
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CRAC (calcium release-activated Ca2+) channels attain an extremely high selectivity for Ca2+ from the blockade of monovalent cation permeation by Ca2+ within the pore. In this study we have exploited the blockade by Ca2+ to examine the size of the CRAC channel pore, its unitary conductance for monovalent cations, and channel gating properties. The permeation of a series of methylammonium compounds under divalent cation-free conditions indicates a minimum pore diameter of 3.9 Å. Extracellular Ca2+ blocks monovalent flux in a manner consistent with a single intrapore site having an effective Ki of 20 μM at −110 mV. Block increases with hyperpolarization, but declines below −100 mV, most likely due to permeation of Ca2+. Analysis of monovalent current noise induced by increasing levels of block by extracellular Ca2+ indicates an open probability (Po) of ∼0.8. By extrapolating the variance/mean current ratio to the condition of full blockade (Po = 0), we estimate a unitary conductance of ∼0.7 pS for Na+, or three to fourfold higher than previous estimates. Removal of extracellular Ca2+ causes the monovalent current to decline over tens of seconds, a process termed depotentiation. The declining current appears to result from a reduction in the number of active channels without a change in their high open probability. Similarly, low concentrations of 2-APB that enhance ICRAC increase the number of active channels while open probability remains constant. We conclude that the slow regulation of whole-cell CRAC current by store depletion, extracellular Ca2+, and 2-APB involves the stepwise recruitment of silent channels to a high open-probability gating mode.
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Eisner, G. M., I. Yamaguchi, R. A. Felder, L. D. Asico, and P. A. Jose. "Role of renal dopamine D1 receptors in natriuresis induced by calcium channel blockers." American Journal of Physiology-Renal Physiology 267, no. 6 (December 1, 1994): F965—F970. http://dx.doi.org/10.1152/ajprenal.1994.267.6.f965.
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The direct tubular natriuretic effect of calcium channel blockers (CCBs) may be due to an interaction between CCBs and a renal tubular dopamine receptor. We therefore studied the effects of two chemically unrelated CCBs, diltiazem and isradipine, infused into the right renal artery of 5% saline-loaded anesthetized rats alone or in the presence of a D1 antagonist, SKF-83742. Isradipine (0.03 microgram.kg-1.min-1) or diltiazem (20 but not 10 micrograms.kg-1.min-1) alone produced an increase in urine flow and an approximate doubling of absolute and fractional sodium excretion, which was not seen in the left kidney or in the control animals (analysis of variance, Scheffe's test, P < 0.05). SKF-83742 alone given systemically or into the right renal artery did not affect these parameters but did block the actions of diltiazem or isradipine. There was no change in mean arterial pressure, renal blood flow, or glomerular filtration rate in any of the experiments. In additional studies, we found that a combined infusion of dopamine (0.1 microgram.kg-1.min-1) and diltiazem (10 micrograms.kg-1.min-1) (doses that by themselves did not alter renal function) produced a twofold or greater increase in urine flow and absolute and fractional sodium excretion; glomerular filtration rate was not significantly changed. Intrarenal arterial CCBs, without a change in renal hemodynamics, produce a natriuresis that is blocked by a D1 antagonist. Concomitant administration of diltiazem and dopamine (each in subeffective doses when used alone) produces a synergistic effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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Hallberg, Pär, Julia Nagy, Malgorzata Karawajczyk, Leif Nordang, Gunilla Islander, Pia Norling, Hans-Erik Johansson, et al. "Comparison of Clinical Factors Between Patients With Angiotensin-Converting Enzyme Inhibitor–Induced Angioedema and Cough." Annals of Pharmacotherapy 51, no. 4 (November 26, 2016): 293–300. http://dx.doi.org/10.1177/1060028016682251.
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Background: Angioedema is a rare and serious adverse drug reaction (ADR) to angiotensin-converting enzyme (ACE) inhibitor treatment. Dry cough is a common side effect of ACE inhibitors and has been identified as a possible risk factor for angioedema. Objective: We compared characteristics between patients with ACE inhibitor–induced angioedema and cough with the aim of identifying risk factors that differ between these adverse events. Methods: Data on patients with angioedema or cough induced by ACE inhibitors were collected from the Swedish database of spontaneously reported ADRs or from collaborating clinicians. Wilcoxon rank sum test, Fisher’s exact test, and odds ratios (ORs) with 95% CIs were used to test for between-group differences. The significance threshold was set to P <0.00128 to correct for multiple comparisons. Results: Clinical characteristics were compared between 168 patients with angioedema and 121 with cough only. Smoking and concomitant selective calcium channel blocker treatment were more frequent among patients with angioedema than cough: OR = 4.3, 95% CI = 2.1-8.9, P = 2.2 × 10-5, and OR = 3.7, 95% CI = 2.0-7.0, P = 1.7 × 10-5. Angioedema cases were seen more often in male patients (OR = 2.2, 95% CI = 1.4-3.6, P = 1.3 × 10-4) and had longer time to onset and higher doses than those with cough ( P = 3.2 × 10-10 and P = 2.6 × 10-4). A multiple model containing the variables smoking, concurrent calcium channel blocker treatment, male sex, and time to onset accounted for 26% of the variance between the groups. Conclusion: Smoking, comedication with selective calcium channel blockers, male sex, and longer treatment time were associated with ACE inhibitor–induced angioedema rather than cough.
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Harutyunyan, K. R., K. V. Melkumyan, H. T. Abrahamyam, S. H. Adamyan, D. H. Khudaverdyan, and A. S. Ter-Markosyan. "Calcium-regulating hormonal system in cardiac functional activity." NEW ARMENIAN MEDICAL JOURNAL, no. 4 (2022): 54–63. http://dx.doi.org/10.56936/18290825-2022.16.4-54.
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The variance of calcium homeostasis is known as a risk factor for the development of heart failure. A study of calcium-regulating hormones is a crucial element to understand underlying pathophysiological mechanisms of heart failure. Pro-inflammatory factors, released during mechanical, hypoxic or bacterial damage of myocardial cells, lead to an imbalance of calcium and disrupt to heart function. The investigation of mentioned factors influence mechanism on the heart, is an urgent solution for preventing the development of heart failure. Present study aimed to reveal the role of calcium-regulating hormones in heart functional activity and their possible involvement in the development of heart failure. The pharmacological analysis of the action mechanism of bacterial lipopolysaccharides on heart functional activity was carried out using a calcium channel blocker. The concentrations of calcium-regulating hormones in blood serum in patients suffering from heart failure was determined by immunoassay enzyme method, and ionized calcium and inorganic phosphate concentrations - by spectrophotometric method. The photoelectrical method was used to determine the direct effect of calcium-regulating hormones and possible calcium-dependent action mechanism of bacterial lipopolysaccharides on the isolated frog’s heart. Clinical findings show that chronic heart failure is accompanied by shifts in the calcium-regulating hormonal system and blood electrolyte balance. In vitro experiments on isolated frog hearts have shown the potentiating effect of parathyroid hormone, its related protein, calcitonin, and vitamin D3 on myocardial contractility. It has been shown, that bacterial lipopolysaccharides suppress the contractile and rhythmogenic functions of the myocardium, and their action can be mediated through a calcium-dependent mechanism. The increase of parathyroid hormone in chronic heart failure has a protective significance aimed at maintaining the contractile ability of a weakened myocardium and preserving cardiac output. Bacterial lipopolysaccharides are able to suppress functional activity of the heart by calcium-dependent mechanism.
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Barrett, Ravina, and James Hodgkinson. "Impact of the COVID-19 pandemic on cardiovascular heart disease medication use: time-series analysis of England’s prescription data during the COVID-19 pandemic (January 2019 to October 2020)." Therapeutic Advances in Cardiovascular Disease 16 (January 2022): 175394472211371. http://dx.doi.org/10.1177/17539447221137170.
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Background: Management of high blood pressure (BP) typically requires adherence to medication regimes. However, it is known that the COVID-19 pandemic both interrupted access to some routine prescriptions and changed some patient health behaviours. Aim: This study, therefore, retrospectively investigated prescription reimbursement of cardiovascular (CVD) medicines as a proxy measure for patient adherence and access to medicines during the pandemic. Methods: A cohort study of all primary care patients in England prescribed CVD medicines. The exposure was to the global pandemic. Prescriptions were compared before and after the pandemic’s onset. Statistical variation was the outcome of interest. Results: Descriptive statistics show changes to monthly prescriptions, with wide confidence intervals indicating varying underlying practice. Analysis of variance reveals statistically significant differences for bendroflumethiazide, potassium-sparing diuretics, nicorandil, ezetimibe, ivabradine, ranolazine, colesevelam and midodrine. After the pandemic began (March–October 2020), negative parameters are observed for ACE inhibitors, beta-blockers, calcium channel blockers, statins, antiplatelet, antithrombotics, ARBs, loop diuretics, doxazosin, bendroflumethiazide, nitrates and indapamide, indicating decelerating monthly prescription items (statistically significant declines of calcium channel blockers, antithrombotic, adrenoreceptor blockers and diuretics) of CVD medicines within the general population. Many data points are not statistically significant, but fluctuations remain clinically important for the large population of patients taking these medications. Conclusion: A concerning decline in uptake of CVD therapies for chronic heart disease was observed. Accessible screening and treatment alongside financial relief on prescription levies are needed. A video abstract is (4 min 51 s) available: https://bit.ly/39gvEHi
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Harding, S. E., S. M. Jones, P. O'Gara, G. Vescovo, and P. A. Poole-Wilson. "Reduced beta-agonist sensitivity in single atrial cells from failing human hearts." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 4 (October 1, 1990): H1009—H1014. http://dx.doi.org/10.1152/ajpheart.1990.259.4.h1009.
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Human myocytes were isolated from right atrial appendage, and contractile responses to inotropic agents were studied. Responses to inotropic agents of cells isolated from patients with mild heart disease [New York Heart Association (NYHA) classes I and II] were compared with those of myocytes from rabbit atria. Maximally effective concentrations of calcium, forskolin, and isoproterenol increased contraction amplitude to a similar extent (11.9, 11.5, and 11.3% change in cell length, respectively), but histamine produced a smaller effect (7.1%). The maximum responses of rabbit atrial cells to calcium (18.5%) and isoproterenol (15.0%) were significantly greater than human. In human cells, the velocity of contraction or relaxation was accelerated more by isoproterenol (P less than 0.05) or forskolin (P less than 0.01) than by high calcium. Only relaxation velocity was increased by isoproterenol in rabbit cells (P less than 0.05). Rabbit myocytes contracted and relaxed 10-30% faster than human (P less than 0.05). Cells from the atria of patients with New York Heart Association (NYHA) heart failure class III or IV were less responsive to isoproterenol than those from class I or II (P less than 0.01). Omitting data from patients who had been taking calcium-channel blockers or beta-adrenoceptor agonist or antagonist drugs did not affect the conclusions. Analysis of variance revealed a significantly greater between-patient than within-patient variation (P less than 0.001), indicating that cells from the same patient have a tendency to respond in a similar way. Responses to high calcium did not differ among NYHA classes. The effect of forskolin was not reduced in NYHA class III, although there was a decreased response in cells from two patients in NYHA class IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Dissertations / Theses on the topic "Calcium channel variance"
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O'Brien, N. L. "Bipolar disorder related functional variants in the calcium channel gene family." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1476756/.
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Bipolar disorder (BD) is a common highly heritable disorder. The calcium channel gene family has been widely implicated in BD aetiology and these genes include CACNA1C, and CACNG4. The association signal for CACNA1C with BD is located in the middle of the third intron of the gene. CACNG4 encodes a transmembrane AMPA receptor regulator that is involved in trafficking AMPA receptors to the neuronal post-synaptic density. High-resolution melting curve (HRM) analysis and whole genome sequencing (WGS) methods were used to identify functional variants in calcium channels genes in the UCL BD cohort. Variants that were predicted to impact gene regulation, transcription or to be damaging to protein structure were genotyped in the larger UCL BD and control cohort. HRM analysis identified 26 calcium channel gene variants. These included two non-synonymous CACNG4 variants that were associated with mental illness (rs371128228, p=1.05x10-4, OR=4.39 and 17:65026851 (C/T), p=5x10-4, OR=9.52). Fluorescent activated cell sorting analysis was used to determine the effect of rs371128228 on trafficking of GluR1 and GluR2 to the cell surface. This analysis demonstrated that the risk allele of rs371128228 significantly decreased cell surface trafficking of GluR1 (p=0.026) but no effect was observed on GluR2 trafficking. WGS analysis of CACNA1C intron 3 identified two BD associated (p=0.015, OR=1.15) variants 105bp apart that were in complete LD. Both variants are predicted to create YY1 transcription factor binding sites. Luciferase reporter assays show a significant decrease in gene expression in the presence of both variants (p=0.004). Protein-DNA complex assays of the CACNA1C variants demonstrate increased nuclear proteins binding affinity for the variant alleles. If these calcium channel variants are confirmed to be important risk factors for BD they could be used as markers for personalised treatment or in the identification of genetic subtypes of BD or other psychiatric illness.
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Lana, B. "The voltage-gated calcium channel α₂δ-1 subunit : splice variants and interacting proteins." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1393281/.
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á2ä-1 is an auxiliary subunit of the voltage-gated calcium channels, and it regulates the trafficking and functions of the channel complex. á2ä-1 subunits contain the binding site for gabapentin (GBP), used for the treatment of neuropathic pain. The first aim of this thesis was to determine whether important functional properties of á2ä-1, such as the ability to regulate calcium currents and binding to GBP, were altered by alternative splicing events on á2ä-1. In addition, the distribution of á2ä-1 splice variants in dorsal root ganglia (DRGs) of naive and spinal nerve ligated (SNL) rats was analysed by RT-PCR and gel electrophoresis. The results obtained from [3H]-GBP binding experiments identified two splice variants characterised by a low binding affinity to GBP. One of those, which is known to undergo up-regulation in DRGs neurons upon SNL, was found to be specifically expressed in smaller neurons, which are normally nociceptive. The interaction of endogenous ligands with á2ä-1 can also contribute to influence the the binding affinity of GBP to á2ä-1. Therefore, the other goal of this study was to analyse the interaction of endogenous ligands with á2ä-1. First, co-immunoprecipitation and radioligand binding experiments demonstrate that á2ä-1 interacts with thrombospondins (secreted proteins that bind á2ä-1 and promote synaptogenesis) and that this interaction reduces the binding affinity of GBP to á2ä-1. Secondly, it was investigated wheather another protein: the low-density lipoprotein receptor (LDLR)-related protein-1 (LRP1) could also interact with á2ä-1 and TSP. It was found that LRP1 co-immunoprecipitates with TSP4 and it also decreases the amount of GBP binding to á2ä-1, suggesting that LRP1 might be involved in promoting the interaction between á2ä-1 and TSP4. These studies have shown that the existence of alternative splice variants of á2ä-1 and the interaction of á2ä-1 with endogenous interactors like TSPs and LRP1 affect the functionality of these subunits. An altered functionality might play an important role upon nerve damage, when á2ä-1 becomes up-regulated, because GBP requires binding to á2ä-1 to exert its therapeutic effect.
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Coghill, Lorraine Sheila. "Regulation of large conductance calcium- and voltage-activated potassium (BK) channel splice variants by protein kinase A." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23309.
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Waheed, Zeina. "Characterization of the +SSTR and ΔSSTR splice variants of the Cav2.1 P/Q-type voltage-gated calcium channel." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55060.
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Cav2.1 P/Q-type voltage-gated calcium channels are essential for neurotransmission in many regions of the mammalian central nervous system (CNS). Alternative splicing generates functional diversity between Cav2.1 splice isoforms and is thought to be a mechanism by which fine-tuning and complexity of Cav2.1-mediated activities occur. The Cav2.1 +SSTR splice variant, located in the S3-S4 linker of domain III, has been identified in rodent brain although its effects on the biophysical and pharmacological properties of Cav2.1 have not been previously studied. Here, by performing splice variant-specific quantitative real-time PCR on selected regions of the rat CNS I demonstrate that +SSTR variant channels are differentially expressed spatially with predominant expression in the brainstem, reticular thalamus and spinal cord. Using whole-cell patch-clamp electrophysiology performed on transfected HEK 293 cells I have shown that compared to ΔSSTR channels, +SSTR variants exhibit faster activation kinetics and a hyperpolarizing shift in the voltage-dependence of activation and inactivation. Additionally, the +SSTR and ΔSSTR variants respond differently to increasing durations of action potential waveforms (APWs) with the charge transference through +SSTR channels being significantly less sensitive to APW broadening than ΔSSTR channels. Together, these data suggest that the unique biophysical properties of the Cav2.1 splice variants contribute to distinct roles in CNS synaptic physiology by relaying different types of action potential-encoding synaptic information. Lastly, I examined whether the +SSTR variant affected the sensitivity of Cav2.1 to the gating modifier peptide toxin ω-Agatoxin-IVA. Using whole-cell patch-clamp electrophysiology I found that the effects of ω-Agatoxin-IVA on current block did not significantly differ between the +SSTR and ΔSSTR splice variants suggesting that SSTR insertion does not affect the binding of ω-Agatoxin-IVA to Cav2.1 channels. The differential expression of Cav2.1 splice variants and their unique channel properties provides insight into the mechanisms by which complexity of P/Q-type calcium channel-mediated signaling contributes to CNS physiology.Medicine, Faculty of
Graduate
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Chai, Shin Luen Chai. "Novel Genetic Modifiers in a Monogenic Cardiac Arrhythmia." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1516618028568975.
Full textBooks on the topic "Calcium channel variance"
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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.
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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Langer, Thomas, and Pietro Caironi. Pathophysiology and therapeutic strategy of respiratory alkalosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0114.
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Respiratory alkalosis is a condition characterized by low partial pressure of carbon dioxide and an associated elevation in arterial pH caused by an imbalance between CO2 production and removal, in favour of the latter. Conditions that cause increased alveolar ventilation, without having a reduction in pH as input stimulus, will cause hypocapnia associated with a variable degree of alkalosis. The major effect of hypocapnia is the increase in pH (alkalosis) and the consequent shift of electrolytes that occurs in relation to it. As a general law, in plasma, anions will increase, while cations will decrease. The acute reduction in ionized calcium, due to the change in extracellular pH, may cause neuromuscular symptoms ranging from paraesthesias, to tetany and seizures. The effect on urine is an increase in urinary strong ion difference/urinary anion gap and a consequent increase in urinary pH. Finally, acute hypocapnic alkalosis causes a constriction of cerebral arteries that can lead to a reduction of cerebral blood flow. The clinical approach to respiratory alkalosis is usually directed toward the diagnosis and treatment of the underlying clinical disorder.
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Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.
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Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
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Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.
Full textAbstract:
Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
Book chapters on the topic "Calcium channel variance"
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Yeow, Sean Qing Zhang, Kelvin Wei Zhern Loh, and Tuck Wah Soong. "Calcium Channel Splice Variants and Their Effects in Brain and Cardiovascular Function." In Ion Channels in Biophysics and Physiology, 67–86. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4254-8_5.
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Kung, Annie W. C., and C. L. Cheung. "Thyrotoxic Periodic Paralysis." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 462–65. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0055.
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Thyrotoxic periodic paralysis (TPP) is a condition featuring attacks of muscle weakness in the presence of hyperthyroidism. Hypokalaemia is the hallmark of TPP. The condition may be life-threatening if there is weakness of respiratory muscles or cardiac arrhythmias. If hyperthyroidism is uncontrolled, TPP is recurrent in nature. The condition has been linked with genetic mutations or variants in certain ion channels that code for sodium and potassium across cell membranes. The main ones are the KCNJ family and L-type calcium channel alpha 1 subunit. The abnormality in these ion channels leads to shifts of potassium across cell membrane in hyperthyroid state.
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Dooren, Sonia Van, Dorien Daneels, Gudrun Pappaert, Maryse Bonduelle, and Pedro Brugada. "Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—Brugada syndrome." In ESC CardioMed, 679–82. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0151.
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The heritable arrhythmogenic disorder Brugada syndrome (BrS), a cardiac ion channelopathy first described in 1992, is inherited as an autosomal dominant trait characterized by incomplete penetrance, variable expression, and phenotypic overlap. These characteristics all complicate the elucidation of the underlying molecular genetic pathway. Clearly, SCN5A, the gene encoding the pore-forming alpha subunit of the cardiac sodium channel, is the major susceptibility gene associated with BrS: 20–30% of BrS patients harbour pathogenic variants in this gene and BrS patients have a more than eight times higher burden of rare variants in this gene compared to controls. Rare pathogenic variants have also been reported in several sodium, potassium, and calcium channel genes, pacemaker genes, and sodium channel interacting genes. Given the minor collective contribution of these additional BrS-associated genes to the total genetic diagnostic yield, the hypothesis has been raised that other (genetic) determinants are involved. Indeed, the monogenic nature of BrS has been questioned and more support has recently been gained for the hypothesis of a complex inheritance based on genome-wide and gene panel studies. Probably, the BrS inheritance pattern is a continuum ranging from a monogenic, over an oligogenic towards even a polygenic spectrum. This, however, further impedes the interpretation of the contribution of (likely) pathogenic variants to the phenotype and urges for a cautious policy in a prenatal and preimplantation genetic diagnostic context: in many cases disease prevention will imply a risk reduction instead of an elimination of disease (development).
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Nurnberger, John I. "General genetics of bipolar disorder." In The Bipolar Brain, 200–222. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197574522.003.0011.
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It has been known for centuries that major mood disorders, including bipolar disorder, cluster in families. The heritability of bipolar disorder appears to be about 85%. Some of that heritability can now be assigned to specific common genetic variants identified in genome-wide association studies and specific rare variants identified in sequencing studies. Some key areas for ongoing investigation include calcium channel–related genes, variants related to synaptic transmission, and markers of neuronal growth and development. Genetic counseling is now based on empirical risk figures from family studies but may in the future be aided by genetic measures such as polygenic risk scores and/or screening for rare variants.
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Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006.
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Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
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Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006_update_001.
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Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
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Lanza, Gaetano Antonio, and Antonio De Vita. "Chronic stable angina." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Alexander Niessner, Sven Wassmann, and Udo Sechtem, 91–106. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0006_update_002.
Full textAbstract:
Treatment of patients with chronic stable angina has two main objectives: to improve clinical outcome and to reduce angina symptoms. Prognosis is mainly improved by a reduction in cardiovascular risk factor burden, which may be achieved by appropriate lifestyle changes and, for some risk factors (e.g. hypercholesterolaemia, hypertension, diabetes), appropriate pharmacological therapy (including, in particular, statins and renin–angiotensin–aldosterone system inhibitors) and use of antithrombotic agents. Symptoms can be improved by a variable combination of traditional (beta-blockers, calcium channel blockers, nitrates) and novel (e.g. ivabradine, ranolazine) anti-ischaemic drugs, which may act through reduction in myocardial oxygen consumption and/or improvement of myocardial perfusion.
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Sklar, Pamela. "Genetics of Schizophrenia and Bipolar Disorder." In Neurobiology of Mental Illness, edited by Pamela Sklar, 232–46. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0018.
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Schizophrenia and bipolar disorder are the classic psychotic disorders. Both diseases are strongly familial, but have proven recalcitrant to genetic methodologies for identifying the etiology until recently. The explosion of strong and convincing genetic evidence indicates a contribution of many DNA changes to the risk of becoming ill. For schizophrenia, there are large contributions of rare copy number variants and common single nucleotide variants, with an overall highly polygenic genetic architecture. There is a role for rare single nucleotide variation as well as de novo genetic variation being pointed to in new sequencing studies, but their overall contribution to risk is less clear. For bipolar disorder, the role of copy number variation appears to be much less pronounced. Specific common single nucleotide polymorphisms are associated, there is evidence for polygenicity and as yet no deep sequencing surveys have been published. Several intriguing biological pathways are suggested by these genetic findings related to microRNAs and calcium channel signaling. Several surprises have emerged from the genetic data that indicate there is significantly more molecular overlap in copy number variants between autism and schizophrenia, and in common variants between schizophrenia and bipolar disorder. Translating these results into biological and etiological understanding has not yet advanced, and will likely only do so when experimental methods are developed than can address the large numbers of genes and variants within them that, along with environmental and stochastic effects, result in the development of disease for a particular person.
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Bardin, Thomas, and Tilman Drüeke. "Renal osteodystrophy." In Oxford Textbook of Rheumatology, 1274–82. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149_update_001.
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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Drüeke, Tilman, and Thomas Bardin. "Renal osteodystrophy." In Oxford Textbook of Rheumatology, 1274–82. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149_update_002.
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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. Its main clinical expression is an increased propensity for fractures. It has been divided into several pathological entities based on histomorphometry criteria of bone turnover, mineralization and volume. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and α-klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can be schematically divided into three main types by histology: (1) osteitis fibrosa reflecting secondary hyperparathyroidism (sHP) is a high bone turnover disease which can develop early in CKD; (2) adynamic bone disease (ABD), at present the predominant type of ROD in dialysis patients, which is mainly the result of PTH resistance or excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone-specific alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus increases only in advanced CKD (stages G4-G5). Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage renal disease is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol, and in addition calcimimetics in dialysis patients, can be used to halt its progression.
Conference papers on the topic "Calcium channel variance"
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Decousus, H. A., M. F. Scully, J. Reynaud, E. Arnaud-Crozat, C. Boissier, R. Barral, P. Queneau, J. Reynaud, C. Parker, and v. v. Kakkar. "CIRCADIAN CHANGES IN THE ANTICOAGULANT EFFECT OF HEPARIN. PHARMACODYNAMIC AND PHARMACOKINETIC EFFECT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644175.
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Six patients, with thromboembolic arterial disease, were prospectively studied to assess the influence of the time of injection of a constant dose of calcium heparin (Choay ), given subcutaneously, on the level of heparin measured by APTT and anti-Xa assay. For each patient, the initial dose of heparin was adjusted by APTT 6h after a morning injection to 1.5 and 2.5 times control. Dose was then kept constant. Four randomized times of injection were tested (8am, 4pm, 8pm and 12pm), in each patient acting as his own control. Blood was sampled via a cannula, at Oh, 2h, 3h,4h,5h,6h, 8h, lOh and 12h after injection. The mean APTT and anti-Xa values for the evening injections (8pm and 12pm) were higher than for the morning injection (8am), at 2h until lOh after injection. These differences were significant (analysis of variance:p<0.001) and reached almost 30 seconds for mean APTT values measured 4h, 5h and 6h after injection. For the afternoon injection (4 pm) the mean APTT and anti-Xa values were intermediate but significantly different from all the other times of injection (analysis of variance: p<0.01).Blood was sampled also on two consecutive days at 12am and 12pm from eight patients receiving heparin subcutaneously for treatment of DVT (administered at 6am and 6pm respectively). Heparin levels by APTT, TT and three antifactor Xa methods (Heptest, Hepaclot, Chromogenic) were significantly higher at night than morning (analysis of variance p<0.005). Cosinor analysis confirmed these results are consistent with circadian variation as we have previously reported after continuous infusion of UF heparin (Br. Med. J., 1985, 290, 341-344). The observed variation was found to be a resultant of a pharmacodynamic effect (circadian variation in assay response to heparin) and pharmacokinetic effect (circadian variation in 99m Tc-heparin clearance). Such circadian variation should be taken into account when deciding heparin dosage.
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Ness, Giulia, Ken Stuart Sorbie, Ali Hassan Al Mesmari, and Shehadeh Masalmeh. "The Impact of CCUS for Improved Oil Recovery on CaCO3 Scaling Potential of Produced Fluids." In SPE EuropEC - Europe Energy Conference featured at the 83rd EAGE Annual Conference & Exhibition. SPE, 2022. http://dx.doi.org/10.2118/209676-ms.
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Abstract Unlike other CCUS technologies, CO2 EOR has been widely implemented at a commercial level and on an industrial scale. In CO2 EOR, CO2 can be injected on its own or alternated with water in CO2 WAG (water-alternating-gas). Both applications have a direct impact on produced fluid compositions influencing GOR, water cut, CO2 concentration and consequently Ca2+, alkalinity and pH. The variation of fluid compositions has an inevitable impact on the scaling potential of produced fluids and on the resulting level of scale formation and its mitigation strategy. The aim of this work is to investigate the scaling potential changes for a wide range of CO2 WAG scenarios in a high salinity carbonate reservoir in the Middle East using input data from reservoir modelling simulations and running multiple sensitivity studies. The main scale formed in this reservoir is calcium carbonate (CaCO3). The equilibrium reservoir water, the produced water chemistry profiles from downhole to stock tank and the scaling risk profiles are modelled using a commercial integrated PVT and aqueous phase software. A rigorous scale prediction procedure previously published by the authors is applied to accurately calculate scale risk trends for variable production scenarios. As CO2 increases in the WAG cycle, reservoir pH drops but the equilibrium with CaCO3 rock causes an increase in alkalinity. This results in more CaCO3 precipitation in the production system where pressure drops and CO2 flashes off solution. Hence, these results show unequivocal detrimental impact of CO2 WAG on the calcium carbonate scaling potential of produced fluids. This leads to a need for operational and/or chemical adjustments to the scale management program when this technology is deployed. Whilst in this field some CaCO3 scale is predicted to form downhole, but this is not a severe problem although it may need to be addressed. The separator is operated at a sufficiently high pressure that calcium carbonate is not expected to form there. Changing operating pressures and CO2 and H2S concentrations can shift some of the problem to the separator, but if this remains at high pressure there will be no scale precipitation here. However, the calcium carbonate scale will predominantly precipitate at stock tank conditions. Implementing green technologies such CCUS is fundamental to achieving net zero goals and this work clearly shows that actions need to be taken to manage the associated CaCO3 scale problems in the produced fluids to make this application successful.
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Rafeeque, Ameena, and Mohammed Fasihul Alam. "The effect of Renin Angiotensin System Blockers versus Calcium Channel Blockers on Progression towards Hypertensive Chronic Kidney Disease: A comprehensive systematic review based on Randomized Controlled Trials." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0162.
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Background: Decline in estimated Glomerular filtration rate (eGFR) is associated with further progression of chronic kidney disease. Evidence suggests that Renin Angiotensin System blockers (RAS), which can be angiotensin-receptor blockers (ARBs) or Angiotensin converting enzymes Inhibitors (ACEIs), have reno- protective effect, but results are variable. Similarly, effects of Calcium channel blockers (CCBs) are shown to have a role in protecting renal function but differ across studies. Hence, the relative effect of ARBs or ACEIs as well as CCBs, and their administration as monotherapy, remain uncertain. Purpose: To summarize and determine the pooled effect of RAS versus CCBs on progression towards hypertensive CKD amongst diabetic as well as non-diabetic patients with CKD of any stage from I-IV. Data sources: All language studies in PubMed, the Cochrane Library Central, Clinical Registry of unpublishedTrials, WHO, Embase, Scopus, ProQuest, reference lists, and expert contacts up to September 2019. Study selection: This study included all the full text articles that studied diabetic and non-diabetic patients with eGFR ≥ 15 ml/min per 1.73m3 or Urinary albumin excretion levels (UAE) ≤ 300mg/d during RAS based treatment an intervention in direct comparison with CCBs treatment based approach as comparator at baseline and at the end of follow-up. However, pooling of all the included studies using meta-analysis was not feasible due to substantial study heterogeneity and the small number of included studies that are meta-analyzable. So, studies were selected for systematic review, and out of which, all the meta-analyzable studies were quantitatively analyzed on the basis of main outcomes such as (i) Relative risk for CKD progression and (ii) Mean differences in SBP and DBP for both the arms. Doi plot and funnel plot were used for detection of publication bias. Results: Review with seven included trials, and metaanalysis using IVhet model was done on three studies for primary CKD outcome and four studies for secondary BP outcomes. RAS blockers and CCBs did not show any statistically significant differences in terms of its effects on further progression CKD with RR of 0.90 [95% CI 0.69, 1.16]. Moreover, there was no statistically significant difference in BP from baseline to final end points between CCBs and RAS inhibitors with WMD of -2.09 mmHg [95% CI -5.96, 1.79] for mean SBP change and -0.71 mmHg [95% CI -2.16, 0.73] for mean DBP change. Conclusion: Evidence asserts no difference between RAS and CCB concerning the risk of progression for CKD and in terms of mean BP differences. However, the study have its own set of limitations due to which more well designed and well conducted RCTs with robust findings are required to confirm the inferences based on this review.
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Ness, Giulia, Kenneth S. Sorbie, Mark Gough, Rifky Akbar, Jonathan J. Wylde, and Alex Thornton. "Application of a Rigorous Scale Prediction Workflow to the Analysis of CaCO3 Scaling in an Extreme Acid Gas, High Temperature, Low Watercut Onshore Field in Southeast Asia." In ADIPEC. SPE, 2022. http://dx.doi.org/10.2118/211312-ms.
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Abstract Calcium carbonate is a pH dependent inorganic mineral scale that is influenced by CO2 and H2S partitioning. CaCO3 prediction must therefore include accurate modelling of the aqueous phase and all hydrocarbon phases present. pH dependent scale prediction challenges and the development of a rigorous procedure for generation of more accurate results were previously published. This procedure has now been applied to an onshore oilfield in Southeast Asia for assessment and management of CaCO3 scaling. A rigorous scale prediction workflow was applied to ‘at-risk’ field producers that showed CaCO3 scaling at and/or downstream of the wellhead choke valve (WHCV). By inputting relevant field data into an integrated PVT/scale prediction code and using the correct procedure, it was possible to evaluate scaling potentials. A series of sensitivity studies allowed well ranking based on the predicted severity of their scaling potentials. The approach validated mechanistic hypotheses for scale development in prolific low watercut, ultra-high CO2, sour, high temperature producers. Close matching of predictions with actual wellhead scaling events provided the basis for improved full-field scale management, and strategic targeting of onsite scale mitigation resources. Target field producers exhibited 0.2% to 25% watercut and presented different degrees of scale precipitation at and/or downstream of the WHCVs. Following well scaling potential assessment, each producer was subject to a series of sensitivity studies to identify (i) how scaling changed with time and (ii) provide focus on the key inputs that most impacted predictions. The initial findings, considering measurement errors (normal field variability), were surprising as key input parameters such as gas phase CO2 and produced water calcium ion concentration appeared to show minimal influence on the final scale prediction results for these wells; even more remarkable considering typical production featured very low salinity produced brine and ultra-high CO2 sour field gas. Focus was therefore shifted to field temperatures, pressure profiles and volumetric flow rates. Of importance is that the selection of ‘critical parameters’ is field specific and that the example presented here shows the variability in scale precipitation at different stages of well production, and how the scaling potential (SR and mg/L) must be evaluated together with the predicted daily theoretical mass of scale (kg/d). This is important in the study of wells with such variable water cut. The following paper demonstrates the value of a rigorous and systematic approach to the prediction of CaCO3 scale, which is often investigated using inappropriate or incomplete methodologies. In this work the authors demonstrate how the technique can address and explain important operational issues and provide solid foundations for implementing and indeed improving the field scale management program.
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Cynara, Ailsa Clarissa, Eti Poncorini Pamungkasari, and Bhisma Murti. "The Effects of Iron Tablet Program, Intrapersonal, and Social Factors On Nutrition Intake to Prevent Anemia in Female Adolescents in Yogyakarta." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.02.61.
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Background: Complexity of behavior among adolescents and the effects of various factors on their behavior require a deeper vision on their health-related behavior components. Inadequate intake of calcium-rich foods and low intake of essential vitamins among female adolescents are cases that indicate the need for a change in the feeding behavior among them. This study aimed to examine the effects of iron tablet program, intrapersonal, and social factors on nutrition intake to prevent anemia in female adolescents. Subjects and Method: A cohort retrospective study was carried out in Senior High Schools in Yogyakarta, Indonesia. A sample of 120 female adolescents was selected by purposive sampling. The dependent variable was nutrition intake. The independent variables were iron tablet program, perceived susceptibility, perceived seriousness, and perceived benefit, and family income. The data were collected by questionnaire and analyzed by a multiple logistic regression. Results: Nutrition intake to prevent anemia in female adolescents increased with iron tablet supplementation program (OR= 11.87; 95% CI= 1.70 to 82.76; p= 0.013), high family income (OR= 24.76; 95% CI= 1.96 to 313.22; p= 0.013), high perceived susceptibility (OR= 77.88; 95% CI= 4.12 to 1471.73; p= 0.004), high perceived seriousness (OR= 228.46; 95% CI= 7.08 to 7369.90; p= 0.002), and high perceived benefit (OR= 94.72; 95% CI= 4.87 to 1841.55; p= 0.003). Nutrition intake decreased with high perceived barrier (OR= 0.02; 95% CI= 0.01 to 0.40; p= 0.010). Conclusion: Nutrition intake to prevent anemia in female adolescents increases with iron tablet program, high family income, high perceived susceptibility, high perceived seriousness, and high perceived benefit. Nutrition intake decreases with high perceived barrier. Keywords: anemia, iron tablet, intrapersonal factor, health belief model Correspondence: Ailsa Clarissa Cynara. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: ailsaclarissacynara@student.uns.ac.id. Mobile: 082230233293. DOI: https://doi.org/10.26911/the7thicph.02.61
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Sinha, Supriya, Karol Riofrio, Arthur Walmsley, Nigel Clegg, Stig Sviland-Østre, and Nicolas Gueze. "REAL-TIME 3D IMAGING OF COMPLEX TURBIDITIC RESERVOIR ARCHITECTURE." In 2021 SPWLA 62nd Annual Logging Symposium Online. Society of Petrophysicists and Well Log Analysts, 2021. http://dx.doi.org/10.30632/spwla-2021-0041.
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Siliciclastic turbidite lobes and channels are known to exhibit varying degrees of architectural complexity. Understanding the elements that contribute to this complexity is the key to optimizing drilling targets, completions designs and long-term production. Several methods for 3D reservoir modelling based on seismic and electromagnetic (EM) data are available that are often complemented with outcrop, core and well log data studies. This paper explores an ultra-deep 3D EM inversion process during real-time drilling and how it can enhance the reservoir understanding beyond the existing approaches. The new generation of ultra-deep triaxial EM logging tools provide full-tensor, multi-component data with large depths of detection, allowing a range of geophysical inversion processing techniques to be implemented. A Gauss-Newton-based 3D inversion using semi-structured meshing was adapted to support real-time inversion of ultra-deep EM data while drilling. This 3D processing methodology provides more accurate imaging of the 3D architectural elements of the reservoir compared to earlier independent up-down, right-left imaging using 1D and 2D processing methods. This technology was trialed in multiple wells in the Heimdal Formation, a siliciclastic Palaeocene reservoir in the North Sea. The Heimdal Fm. sandstones are generally considered to be of excellent reservoir quality, deposited through many turbiditic pulses of variable energy. The presence of thin intra-reservoir shales, fine-grained sands, heterolithic zones and calcite-cemented intervals add architectural complexity to the reservoir and subsequently impacts the fluid flow within the sands. These features are responsible for heterogeneities that create tortuosity in the reservoir. When combined with more than a decade of production, they have caused significant localized movement of oil-water and gas-oil contacts. Ultra-deep 3D EM measurements have sensitivity to both rock and fluid properties within the EM field volume. They can, therefore, be applied to mapping both the internal reservoir structure and the oil-water contacts in the field. The enhanced imaging provided by the 3D inversion technology has allowed the interpretation of what appears to be laterally stacked turbidite channel fill deposits within a cross-axial amalgamated reservoir section. Accurate imaging of these elements has provided strong evidence of this depositional mechanism for the first time and added structural control in an area with little or no seismic signal.
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Novotny, Vaclav, Michal Kolovratnik, Monika Vitvarova, and Jana P. Jakobsen. "Analysis and Design of Novel Absorption Power Cycle Plants." In ASME 2016 10th International Conference on Energy Sustainability collocated with the ASME 2016 Power Conference and the ASME 2016 14th International Conference on Fuel Cell Science, Engineering and Technology. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/es2016-59272.
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Absorption Power Cycles (APCs) provide an interesting field within power cycles. The multicomponent mixture with variable temperature across boiling is employed as a working fluid. This has a potential for decreasing exergy loss associated with heat transfer during phase change processes (boiling and condensation). Absorption process has also an effect of lowering exhaust pressure of a turbine. The APCs hold a potential for heat recovery applications at very low temperatures, where constant temperature of boiling and condensation largely limits performance and economic effectiveness of Organic Rankine cycles (ORCs). Theoretical calculations show superiority of APC over extensive range of considered ORC working fluid. The advantage of APC further increases when air cooled condenser needs to be used instead of wet cooling tower. With the same boundary conditions for all cycles the APC provides higher utilization efficiency and power output at source temperatures below approximately 120 °C, for temperatures as low as 60 °C the net power output can be surpassed even more than three times. The proposed APC employs aqueous solution of salts considered generally for absorption cooling (Lithium Bromide, Lithium Chloride, Calcium Chloride) as a working fluid. Unlike ammonia used in mixture with water in Kalina APC or often ORC working fluids, used salts are non-toxic, environmentally friendly and pure water in expander simplifies its design. After summary of theoretical research from thermodynamics point of view are discussed principles, aspects and issues for design of single components of the cycle. Results of sizing are presented on two examples with 100 °C heat source. First one is 20 kWe unit using hot air as a heat source and air cooled condenser, second one is 500 kWe unit with heat source being pressurized water and using wet cooling tower heat rejection. Results show possibility of building relatively efficient system for even small power output with turbine isentropic efficiency nearly 80 % for the 20 kWe unit, but relatively large heat exchangers.
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Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.
Full textAbstract:
Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.