Relevant bibliographies by topics / Calcification

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Calcification'

Author: Grafiati
Published: 4 June 2021
Last updated: 23 November 2024

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Journal articles on the topic "Calcification"

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Gade, Piyusha S., Riikka Tulamo, Kee-won Lee, Fernando Mut, Eliisa Ollikainen, Chih-Yuan Chuang, Bong Jae Chung, et al. "Calcification in Human Intracranial Aneurysms Is Highly Prevalent and Displays Both Atherosclerotic and Nonatherosclerotic Types." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (October 2019): 2157–67. http://dx.doi.org/10.1161/atvbaha.119.312922.

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Objective: Although the clinical and biological importance of calcification is well recognized for the extracerebral vasculature, its role in cerebral vascular disease, particularly, intracranial aneurysms (IAs), remains poorly understood. Extracerebrally, 2 distinct mechanisms drive calcification, a nonatherosclerotic, rapid mineralization in the media and a slower, inflammation driven, atherosclerotic mechanism in the intima. This study aims to determine the prevalence, distribution, and type (atherosclerotic, nonatherosclerotic) of calcification in IAs and assess differences in occurrence between ruptured and unruptured IAs. Approach and Results: Sixty-five 65 IA specimens (48 unruptured, 17 ruptured) were resected perioperatively. Calcification and lipid pools were analyzed nondestructively in intact samples using high resolution (0.35 μm) microcomputed tomography. Calcification is highly prevalent (78%) appearing as micro (<500 µm), meso (500 µm–1 mm), and macro (>1 mm) calcifications. Calcification manifests in IAs as both nonatherosclerotic (calcification distinct from lipid pools) and atherosclerotic (calcification in the presence of lipid pools) with 3 wall types: Type I—only calcification, no lipid pools (20/51, 39%), Type II—calcification and lipid pools, not colocalized (19/51, 37%), Type III—calcification colocalized with lipid pools (12/51, 24%). Ruptured IAs either had no calcifications or had nonatherosclerotic micro- or meso-calcifications (Type I or II), without macro-calcifications. Conclusions: Calcification in IAs is substantially more prevalent than previously reported and presents as both nonatherosclerotic and atherosclerotic types. Notably, ruptured aneurysms had only nonatherosclerotic calcification, had significantly lower calcification fraction, and did not contain macrocalcifications. Improved understanding of the role of calcification in IA pathology should lead to new therapeutic targets.
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Li, Yuan, Changqiu Wang, Anhuai Lu, Kang Li, Xiao Cheng, Chongqing Yang, Yanzhang Li, Yan Li, and Hongrui Ding. "A Comparative Study of Pathological Nanomineral Aggregates with Distinct Morphology in Human Aortic Atherosclerotic Plaques." Journal of Nanoscience and Nanotechnology 21, no. 1 (January 1, 2021): 547–54. http://dx.doi.org/10.1166/jnn.2021.18449.

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Calcification exists in atherosclerotic plaques in the form of nanomineral aggregates and is closely related to the development of atherosclerosis. Spheroidal and massive calcification are two major types of calcification found in atherosclerotic tissue. However, the exact difference between these two types of calcification is still not clear. Samples composed entirely of spheroidal calcifications and massive calcifications were isolated from aortic atherosclerotic plaques and tested using both bulk and microscopic analysis techniques. Scanning electron microscopy and transmission electron microscopy showed that spheroidal calcifications had a core–shell structure. Massive calcifications were composed of randomly arranged nanocrystals. Synchrotron radiation X-ray diffraction, Raman spectroscopy and selected area electron diffraction showed amorphous calcium phosphate, whitlockite and carbonate hydroxyapatite all existing in spheroidal calcification, while massive calcification only consisted of carbonate hydroxyapatite. We conclude that amorphous calcium phosphate may act as a precursor phase of spheroidal calcifications that eventually transforms into a crystalline phase, while whitlockite in lesions could aggravate the progression of atherosclerosis.
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Golüke, Nienke M. S., Enrico Meijer, Emiel A. van Maren, Annemarieke de Jonghe, Mariëlle H. Emmelot-Vonk, Evelien van Valen, Pim A. de Jong, and Huiberdina L. Koek. "Amount and Distribution of Intracranial Calcification in Symptomatic and Asymptomatic Primary Familial Brain Calcification." Neurology: Clinical Practice 13, no. 4 (May 9, 2023): e200163. http://dx.doi.org/10.1212/cpj.0000000000200163.

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Background and ObjectivesIn clinical practice, it can be difficult to differentiate between intracranial calcifications related to primary familial brain calcification (PFBC) or aging. Also, little is known about the consequences of the amount of intracranial calcifications in patients with PFBC. Therefore, we aimed to compare the amount and distribution of intracranial calcifications in persons with PFBC with controls and between asymptomatic and symptomatic PFBC cases.MethodsThis was a case-control study including patients with PFBC and controls. Controls received a CT of the brain because of a trauma and had at least some basal ganglia calcification. The Nicolas score and volume of calcification were used to quantify intracranial calcifications on the CT scans. Receiver operating characteristic curves were obtained to calculate optimal cutoff points to discriminate between cases and controls. Mann-WhitneyUtests and logistic regression, adjusted for age and sex, were used to compare the amount of calcification.ResultsTwenty-eight cases (median age 65 years, 50.0% male) and 90 controls (median age 74 years, 46.1% male) were included. Calcification scores were higher in cases (median volume: 4.91 cm3against 0.03 cm3,p< 0.001, median Nicolas score: 26.5 against 2.0,p< 0.001) than controls. Calcifications were also more diffusely distributed in cases. To differentiate between cases and controls, optimal cutoff points were ≥0.2 cm3for the calcification volume and ≥6.0 for the Nicolas score. Calcification was higher for symptomatic than asymptomatic cases (calcification volume: 13.62 cm3against 1.61 cm3,p= 0.01, Nicolas score: 39.0 against 15.5,p= 0.02). After adjustment for age and sex, the Nicolas score remained significantly higher in symptomatic patients, and the calcification volume did not.DiscussionPatients with PFBC had more severe intracranial calcifications, and these calcifications were more diffusely distributed through the brain compared with controls. Symptomatic patients with PFBC might have more intracranial calcifications than asymptomatic persons.
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Vos, Annelotte, Aryan Vink, Remko Kockelkoren, Richard A. P. Takx, Csilla Celeng, Willem P. T. M. Mali, Ivana Isgum, Ronald L. A. W. Bleys, and Pim A. de Jong. "Radiography and Computed Tomography Detection of Intimal and Medial Calcifications in Leg Arteries in Comparison to Histology." Journal of Personalized Medicine 12, no. 5 (April 29, 2022): 711. http://dx.doi.org/10.3390/jpm12050711.

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Calcifications are common in the tunica intima and tunica media of leg arteries. There is growing interest in medial arterial calcifications, as they may be modifiable with treatment. We aimed to investigate radiography and computed tomography (CT) for the detection and characterization of both types of arterial calcification in leg arteries in relation to histology. In a postmortem study we therefore investigated 24 popliteal and 24 tibial arteries. The reference standard was presence of arterial calcification and the dominance of intimal or medial calcification on histology. Radiographs and CT scans were scored for presence of calcification and for dominant intimal or medial pattern based on prespecified criteria (annularity, thickness, continuity). Both radiography and CT detected 87% of histologically proven calcifications but missed mild calcifications in 13%. When only the arteries with detected calcifications were included, a moderate agreement was observed on intimal/medial location of calcifications between histology and radiography (correct in 19/24 arteries (79%); Kappa 0.58) or CT (correct in 33/46 arterial segments (72%); Kappa 0.48). With both modalities there was a slight tendency to classify intimal calcifications as being located in the media and to miss media calcification. Our study demonstrates the potential and limitations of both radiography and CT to detect and classify arterial calcifications in leg arteries.
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Wu, Baijian, Xuan Pei, and Zhi-Yong Li. "How Does Calcification Influence Plaque Vulnerability? Insights from Fatigue Analysis." Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/417324.

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Background.Calcification is commonly believed to be associated with cardiovascular disease burden. But whether or not the calcifications have a negative effect on plaque vulnerability is still under debate.Methods and Results.Fatigue rupture analysis and the fatigue life were used to evaluate the rupture risk. An idealized baseline model containing no calcification was first built. Based on the baseline model, we investigated the influence of calcification on rupture path and fatigue life by adding a circular calcification and changing its location within the fibrous cap area. Results show that 84.0% of calcified cases increase the fatigue life up to 11.4%. For rupture paths 10Dfar from the calcification, the life change is negligible. Calcifications close to lumen increase more fatigue life than those close to the lipid pool. Also, calcifications in the middle area of fibrous cap increase more fatigue life than those in the shoulder area.Conclusion.Calcifications may play a positive role in the plaque stability. The influence of the calcification only exists in a local area. Calcifications close to lumen may be influenced more than those close to lipid pool. And calcifications in the middle area of fibrous cap are seemly influenced more than those in the shoulder area.
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Sekimoto, Teruo, Takamasa Tanaka, Tatsuya Shiraki, Renu Virmani, and Aloke V. Finn. "How does atherosclerotic plaque become calcified, and why?" AIMS Medical Science 11, no. 4 (2024): 421–38. http://dx.doi.org/10.3934/medsci.2024029.

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<p>Vascular calcification involves the crystallization of calcium/phosphate in the form of hydroxyapatoite in the extracellular matrix of the arterial wall. Vascular calcification is categorized into 3 main etiologies: (1) inflammatory/atherosclerotic (mostly intimal), (2) metabolic (mostly medial), and (3) genetic background (mostly medial). Several overlapping mechanisms trigger all three types of calcifications. Intimal coronary artery calcification simultaneously develops with the progression of atherosclerosis and has been recognized as a surrogate marker of atherosclerotic inflammatory vascular disease. Pathologically, atherosclerotic calcification initially occurs as microcalcifications (0.5 to 15 µm) and results in larger dense calcification, eventually forming sheet calcifications (&gt;3 mm). Among the plaque types, the degree of calcification is the highest in fibrocalcific plaques, followed by healed plaque ruptures, and is the lowest in pathologic intimal thickening. Recent pathologic and imaging-based studies suggest that massive dense calcifications are usually associated with stable plaques, whereas microcalcifications are indicative of vulnerable plaques which may cause acute thrombotic events. Although the mechanisms of calcification are not fully elucidated, apoptotic inflammatory cells and smooth muscle cells, along with the induction of bone formation, play crucial roles in its initiation and progression. A deeper understanding of vascular calcification will improve the risk stratification and patient outcomes through the development of new therapies.</p>
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Sridhar, Sucheta, Yingyue Zhou, Adiljan Ibrahim, Sergio Bertazzo, Tania Wyss, Amanda Swain, Upasana Maheshwari, Sheng-Fu Huang, Marco Colonna, and Annika Keller. "Targeting TREM2 signaling shows limited impact on cerebrovascular calcification." Life Science Alliance 8, no. 1 (October 28, 2024): e202402796. http://dx.doi.org/10.26508/lsa.202402796.

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Brain calcification, the ectopic mineral deposits of calcium phosphate, is a frequent radiological finding and a diagnostic criterion for primary familial brain calcification. We previously showed that microglia curtail the growth of small vessel calcification via the triggering receptor expressed in myeloid 2 (TREM2) in thePdgfbret/retmouse model of primary familial brain calcification. Because boosting TREM2 function using activating antibodies has been shown to be beneficial in other disease conditions by aiding in microglial clearance of diverse pathologies, we investigated whether administration of a TREM2-activating antibody could mitigate vascular calcification inPdgfbret/retmice. Single-nucleus RNA-sequencing analysis showed that calcification-associated microglia share transcriptional similarities to disease-associated microglia and exhibited activated TREM2 and TGFβ signaling. Administration of a TREM2-activating antibody increased TREM2-dependent microglial deposition of cathepsin K, a collagen-degrading protease, onto calcifications. However, this did not ameliorate the calcification load or alter the mineral composition and the microglial phenotype around calcification. We therefore conclude that targeting microglia with TREM2 agonistic antibodies is insufficient to demineralize and clear vascular calcifications.
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Speelman, Lambert, Ajay Bohra, E. Marielle H. Bosboom, Geert Willem H. Schurink, Frans N. van de Vosse, Michel S. Makaroun, and David A. Vorp. "Effects of Wall Calcifications in Patient-Specific Wall Stress Analyses of Abdominal Aortic Aneurysms." Journal of Biomechanical Engineering 129, no. 1 (July 27, 2006): 105–9. http://dx.doi.org/10.1115/1.2401189.

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It is generally acknowledged that rupture of an abdominal aortic aneurysm (AAA) occurs when the stress acting on the wall over the cardiac cycle exceeds the strength of the wall. Peak wall stress computations appear to give a more accurate rupture risk assessment than AAA diameter, which is currently used for a diagnose. Despite the numerous studies utilizing patient-specific wall stress modeling of AAAs, none investigated the effect of wall calcifications on wall stress. The objective of this study was to evaluate the influence of calcifications on patient-specific finite element stress computations. In addition, we assessed whether the effect of calcifications could be predicted directly from the CT-scans by relating the effect to the amount of calcification present in the AAA wall. For 6 AAAs, the location and extent of calcification was identified from CT-scans. A finite element model was created for each AAA and the areas of calcification were defined node-wise in the mesh of the model. Comparisons are made between maximum principal stress distributions, computed without calcifications and with calcifications with varying material properties. Peak stresses are determined from the stress results and related to a calcification index (CI), a quantification of the amount of calcification in the AAA wall. At calcification sites, local stresses increased, leading to a peak stress increase of 22% in the most severe case. Our results displayed a weak correlation between the CI and the increase in peak stress. Additionally, the results showed a marked influence of the calcification elastic modulus on computed stresses. Inclusion of calcifications in finite element analysis of AAAs resulted in a marked alteration of the stress distributions and should therefore be included in rupture risk assessment. The results also suggest that the location and shape of the calcified regions—not only the relative amount—are considerations that influence the effect on AAA wall stress. The dependency of the effect of the wall stress on the calcification elastic modulus points out the importance of determination of the material properties of calcified AAA wall.
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Wen, Jirui, Yali Miao, Shichao Wang, Ruijie Tong, Zhiwei Zhao, and Jiang Wu. "Calcification: A Disregarded or Ignored Issue in the Gynecologic Tumor Microenvironments." International Journal of Gynecologic Cancer 28, no. 3 (March 2018): 486–92. http://dx.doi.org/10.1097/igc.0000000000001185.

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AbstractAlthough calcification in the gynecologic tumor microenvironments is a common phenomenon, doctors and researchers still disregard or ignore the issue. In fact, this change in the gynecologic tumor microenvironments is clinically significant and a number of studies have reported an association between calcification and gynecological tumor progression. In ovarian cancer, calcification is predominantly psammomatous and largely occurs in serous papillary ovarian tumors. In addition, calcification in ovarian cancer correlated with lower histologic grade and may indicate a poorer survival rate. In uterine fibroids, calcification occurs as a degenerative change and is predictive of a good prognosis. As for endometrial cancer and cervical cancer, calcification rarely occurs in these cancers. The mechanism of calcification in the gynecologic tumor microenvironments is not currently clear. One theory is that calcification occurs due to degeneration of the tumor cells; another theory is that calcification occurs in response to secretions from cells in the tumor microenvironment. Although previous studies have revealed a direct association between calcifications and gynecological tumors, this association has not been fully clarified. To better clarify the significance of calcification in terms of diagnosing and treating gynecological tumors, the associations between calcification and the different histologic stages and prognosis in gynecological tumors should be further studied. In particular, more attention should be paid to the morphological characteristics, chemical nature, and mechanism of calcifications in the gynecological tumor microenvironments.
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Zhou, Yuwen, and Qiu Meng. "Bevacizumab associated calcifications might be a prognostic marker in patients with metastatic colorectal cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16108-e16108. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16108.

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e16108 Background: Cetuximab associated calcifications is a positive predictive factor in metastatic colorectal cancer (mCRC). In patients with glioblastoma, bevacizumab-induced calcifications are also related to a better prognosis. However, tumor calcifications are rarely recognized in mCRC patients treated with bevacizumab. This study was to investigate the correlation between clinical outcome and calcification in mCRC who received bevacizumab and chemotherapy as the first-line treatment. Methods: A single retrospective cohort study was conducted with all diagnosed mCRC cases who received bevacizumab and chemotherapy as the first-line therapy in our hospital from January 2016 to January 2019. Clinical variables were retrieved from medical records and tumor calcification were evaluated independently by radiologists on the basis of computed tomography scans. A univariate and multivariate COX regression analysis was performed to evaluate the association between calcification and outcome. Results: 159 patients with an average age of 59.0 years were included. Median follow-up was 29.6 months. Among all enrolled patients, 31 had tumor calcification [31/159 (19.5%)]. The median overall survival (OS) and progression-free survival (PFS) was significantly better in patients with calcification than those without calcification (28.0 vs. 24.9 months, p= 0.024; 12.0 vs. 10.0 months, p= 0.026). A higher objective response rate (61.3% vs. 50.0%) was also observed in calcification group. On multivariate analysis, tumor calcification was independently associated with OS (hazard ratio 1.799, 95% CI 1.002–3.230) and PFS (hazard ratio 1.609, 95% CI 1.013–2.557). Conclusions: Tumor calcification was independently associated with improved prognosis in colorectal cancer. It might be a potential prognostic marker.
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Dissertations / Theses on the topic "Calcification"

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Harper, Glenn Martin. "Calcification in coccolithophores." Thesis, University of Plymouth, 2017. http://hdl.handle.net/10026.1/8664.

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Coccolithophores are uni-cellular phytoplankton and they form an exceedingly diverse group in the phylum Haptophyta. They produce highly complex structures known as coccoliths by a biomineralisation process known as calcification. The first part of the work undertaken was to investigate the process of calcification in the coccolithophore Coccolithus pelagicus using a combination of Transmission Electron Microscopy (TEM), Scanning Electron Microscopy (SEM) and light microscopy techniques. This allowed better understanding of the formation, transit of the coccolith through the cell until its final placing in the coccosphere. The second part of the work looked at the coccolithophore Emiliania huxleyi which is divided into several morphotypes with the two most widely recognised being A and B, it can be further subdivided into further groups according to genotype by Coccolithophore Morphology Motif (CMM). The CMMs lie in the 3/ untranslated region of the coccolith-polysaccharide associated protein-GPA, which is associated with coccolith structure control and they are labelled I, II, III and IV. The work undertaken used a Scanning Electron Microscope (SEM) to investigate the morphologies of homozygous CMM I and CMMIV cell’s coccoliths. This information was used to establish a significant difference between the CMMI cells and CMMIV cells but only at certain locations. The cause for this is possibly as a result of several factors (temperature, salinity, pCO2, Ca availability and light levels) and requires further investigation.
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Desjardins, Lucie. "Marqueurs de risque des complications de la maladie rénale chronique." Thesis, Amiens, 2015. http://www.theses.fr/2015AMIE0013.

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La maladie rénale chronique (MRC) est un problème majeur de santé publique du fait de l’augmentation constante de son incidence et des complications cardiovasculaires fréquemment rencontrées, de même que l’accumulation dans le sang des patients de molécules appelées toxines urémiques. Le but de cette thèse est de déterminer les potentielles associations entre certaines toxines urémiques et certaines techniques non-invasives avec les paramètres biochimiques et vasculaires, la mortalité globale et cardiovasculaire dans une cohorte de patients à différents stades de la MRC. Dans cette étude, nous avons démontré que les taux de chaînes légères libres (CLL), de sclérostine et de β2 microglobuline (β2M) étaient augmentés de manière précoce dans la MRC et culminaient chez les patients dialysés. Seuls les taux de β2M étaient indépendamment associés à la mortalité globale et cardiovasculaire dans notre cohorte et aux événements cardiovasculaires chez les pré-dialysés. De plus, nous avons démontré que la mesure des calcifications vasculaires (en particulier la mesure du score de calcifications coronaires), ajoutait une valeur prédictive de la mortalité globale et des événements cardiovasculaires, à la mesure des facteurs de risque traditionnels (âge, sexe, tabagisme, hypertension et taux de triglycérides).Malgré la taille relativement petite de notre cohorte, les études menées pour cette thèse ont permis de mettre en évidence des marqueurs des complications de la MRC, comme la β2M et la mesure des calcifications vasculaires. Ces marqueurs ajoutés en pratique de routine pourraient améliorer la prédiction du risque cardiovasculaire et de décès dans cette population
Chronic kidney disease (CKD) is a serious public health problem due to the constant increase of its incidence. In particular, CKD patients are at high risk of developing cardiovascular disease further the accumulation of molecules called uremic toxins. The purpose of this thesis was to evaluate risk markers of CKD complications in a cohort of patients at different CKD stages by evaluating some uremic toxins and some non-invasive techniques to determine their potential associations with vascular and biochemical parameters, global and cardiovascular mortality. In this study, we demonstrated that the kappa and lambda free light chain, sclerostin and β2 microglobulin (ß2M) levels were increased in early CKD stage and culminated in dialysis patients. Free light chain and sclerostin levels were associated with inflammation markers but not with vascular parameters. These levels appeared to be associated with mortality, but this association disappeared after adjustment for other factors. On the other side, we have demonstrated that the ß2M levels were independently associated with overall and cardiovascular mortality in our cohort and cardiovascular events in pre-dialysis patients. In addition, we demonstrated that the addition of vascular calcification scores (especially the coronary artery calcification score) to TRFs appears to improve CV risk assessment in a CKD population.This work identified several important markers of CKD complications, as ß2M and measurement of vascular calcification scores. The addition of these two markers in routine practice could improve the prediction of cardiovascular risk and mortality in this population
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Byon, Chang Hyun. "Oxidative stress-stimulated vascular calcification." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/byon.pdf.

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Dhore, Cherida Rachel. "Molecular regulation of vascular calcification." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2005. http://arno.unimaas.nl/show.cgi?fid=6374.

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Walker, Charlotte. "Mechanisms of calcification in coccolithophores." Thesis, University of Southampton, 2018. https://eprints.soton.ac.uk/425508/.

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Coccolithophores are unicellular marine algae characterised by the production of calcite coccoliths. As a result of their calcification they contribute significantly to global biogeochemical cycles. Comprehensive understanding of the mechanisms behind calcification remains elusive, due in part to the research focus on one species, Emiliania huxleyi; the most globally abundant of all coccolithophores. It is imperative to investigate calcification in other species to better understand this biogeochemically important process, especially as the ecological success of E. huxleyi may be due to certain physiological differences with other species. This study set out to explore differences between species in the mechanisms of calcification in three primary areas. Firstly, the physiological requirement for calcification remains poorly understood, particularly as non-calcifying strains of E. huxleyi grow normally in laboratory culture. This study identified a contrast in the requirement for calcification between E. huxleyi and the ecologically important Coccolithus braarudii. Calcification disruption had no negative impacts on E. huxleyi but resulted in major growth defects in C. braarudii demonstrating an obligate requirement for calcification in this species. Secondly, the previous identification of Si transporters in some coccolithophores was further investigated using a combination of physiological and expression studies to identify that Si plays a role in heterococcolith calcification during their diploid life stage. C. braarudii Si transporters were also found to be regulated in response to available Si and shown to be expressed in natural populations. Finally, coccolith associated polysaccharides (CAPs) are an integral component of the calcification mechanism known to modulate the precipitation of calcite. The data presented here show that extracellular CAPs differ in structure and composition between species and that they also play an important role in the organisation of the coccosphere, expanding upon their role and importance in calcification. These findings mark crucial physiological differences between coccolithophore species. The identification of a requirement for calcification in coccolithophores highlights the importance of maintaining a coccosphere. The requirement for Si in some species suggests major physiological differences between species which may influence their ecology. Consequently, these contrasting physiological characteristics may contribute to significant differences in the response of coccolithophores to future ocean conditions.
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Pawade, Tania Ashwinikumar. "Imaging calcification in aortic stenosis." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/29589.

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BACKGROUND Aortic stenosis is a common and potentially fatal condition in which fibro-calcific changes within the valve leaflets lead to the obstruction of blood flow. Severe symptomatic stenosis is an indication for aortic valve replacement and timely referral is essential to prevent adverse clinical events. Calcification is believed to represent the central process driving disease progression. 18F-Fluoride positron emission tomography computed tomography (PET-CT) and CT aortic valve calcium scoring (CT-AVC) quantify calcification activity and burden respectively. The overarching aim of this thesis was to evaluate the applications of these techniques to the study and management of aortic stenosis. METHODS AND RESULTS REPRODUCIBILITY The scan-rescan reproducibility of 18F-fluoride PET-CT and CT-AVC were investigated in 15 patients with mild, moderate and severe aortic stenosis who underwent repeated 18F-fluoride PET-CT scans 3.9±3.3 weeks apart. Modified techniques enhanced image quality and facilitated clear localization of calcification activity. Percentage error was reduced from ±63% to ±10% (tissue-to-background ratio most-diseased segment (MDS) mean of 1.55, bias -0.05, limits of agreement - 0·20 to +0·11). Excellent scan-rescan reproducibility was also observed for CT-AVC scoring (mean of differences 2% [limits of agreement, 16 to -12%]). AORTIC VALVE CALCIUM SCORE: SINGLE CENTRE STUDY Sex-specific CT-AVC thresholds (2065 in men and 1271 in women) have been proposed as a flow-independent technique for diagnosing severe aortic stenosis. In a prospective cohort study, the impact of CT-AVC scores upon echocardiographic measures of severity, disease progression and aortic valve replacement (AVR)/death were examined. Volunteers (20 controls, 20 with aortic sclerosis, 25 with mild, 33 with moderate and 23 with severe aortic stenosis) underwent CT-AVC and echocardiography at baseline and again at either 1 or 2-year time-points. Women required less calcification than men for the same degree of stenosis (p < 0.001). Baseline CT-AVC measurements appeared to provide the best prediction of subsequent disease progression. After adjustment for age, sex, peak aortic jet velocity (Vmax) ≥ 4m/s and aortic valve area (AVA) < 1 cm2, the published CT-AVC thresholds were the only independent predictor of AVR/death (hazard ratio = 6.39, 95% confidence intervals, 2.90-14.05, p < 0.001). AORTIC VALVE CALCIUM SCORE: MULTICENTRE STUDY CT-AVC thresholds were next examined in an international multicenter registry incorporating a wide range of patient populations, scanner vendors and analysis platforms. Eight centres contributed data from 918 patients (age 77±10, 60% male, Vmax 3.88±0.90 m/s) who had undergone ECG-gated CT within 3 months of echocardiography. Of these 708 (77%) had concordant echocardiographic assessments, in whom our own optimum sex-specific CT-AVC thresholds (women 1377, men 2062 AU) were nearly identical to those previously published. These thresholds provided excellent discrimination for severe stenosis (c-statistic: women 0.92, men 0.88) and independently predicted AVR and death after adjustment for age, sex, Vmax ≥4 m/s and AVA < 1 cm2 (hazards ratio, 3.02 [95% confidence intervals, 1.83-4.99], p < 0.001). In patients with discordant echocardiographic assessments (n=210), CT-AVC thresholds predicted an adverse prognosis. BICUSPID AORTIC VALVES Within the multicentre study, higher continuity-derived estimates of aortic valve area were observed in patients with bicuspid valves (n=68, 1.07±0.35 cm) compared to those with tri-leaflet valves (0.89±0.36 cm p < 0.001,). This was despite no differences in measurements of Vmax (p=0.152), or CT-AVC scores (p=0.313). The accuracy of AVA measurments in bicuspid valves was therefore tested against alternative markers of disease severity. AVA measurements in bicuspid valves demonstrated extremely weak associations with CT-AVC scores (r2=0.08, p=0.02) and failed to correlate with downstream markers of disease severity in the valve and myocardium and against clinical outcomes. AVA measurements in bicuspid patients also failed to independently predict AVR/death after adjustment for Vmax ≥4 m/s, age and gender. In this population CT-AVC thresholds (women 1377, men 2062 AU) again provided excellent discrimination for severe stenosis. CONCLUSIONS Optimised 18F-fluoride PET-CT scans quantify and localise calcification activity, consolidating its potential as a biomarker or end-point in clinical trials of novel therapies. CT calcium scoring of aortic valves is a reproducible technique, which provides diagnostic clarity in addition to powerful prediction of disease progression and adverse clinical events.
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Zainuddin. "Synthesis and calcification of hydrogel biomaterials /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18693.pdf.

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Chau, Hien Nguyet 1977. "Renal calcification in Npt2 knockout mice." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=78338.

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Mice homozygous for the disrupted renal type 11a sodium/phosphate (Na/Pi) cotransporter gene, Npt2, (Npt2 KO) exhibit renal Pi wasting and hypercalciuria, predisposing factors for renal stone formation. We observed that Npt2 KO mice, but not wild-type littermates form renal stones. The renal stones were evident in newborn, weanling and adult mice and composed of calcium (Ca) and Pi. The presence of renal calcification correlated with the absence of Npt2 gene expression and the presence of genes responsible for the synthesis (1alpha-hydroxylase) and catabolism (24-hydroxylase) of 1,25-dihydroxyvitamin D, whose elevated levels contribute to the hypercalciuria and renal calcification in Npt2 KO mice. The renal calcification was associated with increased osteopontin (OPN) mRNA expression and colocalized with OPN, the latter associates with renal stones in vivo and inhibits Ca mineralization in vitro). These data demonstrate that hyperphosphaturia and hypercalciuria, secondary to Npt2 gene disruption, are sufficient for the development of renal calcification.
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Rendeiro, Ana Rita Pimentel do Couto. "Genetics and epidemiology of ectopic calcification." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2008. http://hdl.handle.net/10216/54257.

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Promsy, Eric. "Calcification du disque intervertébral chez l'enfant." Montpellier 1, 1988. http://www.theses.fr/1988MON11212.

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Books on the topic "Calcification"

1

Henein, Michael, ed. Cardiovascular Calcification. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-81515-8.

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Aikawa, Elena, and Joshua D. Hutcheson, eds. Cardiovascular Calcification and Bone Mineralization. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-46725-8.

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J, Evans A., ed. Breast calcification: A diagnostic manual. London: Greenwich Medical Media, 2002.

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Steinfort, Joop. The possible role of noncollagenous matrix components in dentin mineralization: The rat incisor as a model. [S.l: s.n.], 1990.

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João Ricardo Mendes de Oliveira. Managing idiopathic basal ganglia calcification ("Fahr's disease"). New York: Nova Science Publishers, 2011.

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Svetlyĭ, L. I. Blokatory medlennykh kalʹt︠s︡ievykh kanalov: Monografii︠a︡. Kursk: Kurskiĭ gos. medit︠s︡inskiĭ universitet, 2006.

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L, Hukins David W., ed. Calcified tissue. Boca Raton, Fla: CRC Press, 1989.

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European Symposium on Calcified Tissues (23rd 1993 Heidelberg, Germany). Abstracts: XXIIIrd European Symposium on Calcified Tissues, April 25-29, 1993, Heidelberg, Germany. New York, NY: Springer International, 1993.

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International Conference on the Chemistry and Biology of Mineralized Tissues (2nd 1984 Gulf Shores, Ala.). The chemistry and biology of mineralized tissues: Proceedings of the Second International Conference on the Chemistry and Biology of Mineralized Tissues, held in Gulf Shores, Alabama, September 9-14, 1984. [S.l: s.n.], 1985.

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Heath, Carolyn Ruth. Calcification of Algal biofilms in hard waters: Occurrence and control. Birmingham: University of Birmingham, 1994.

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Book chapters on the topic "Calcification"

1

Taylor, Alison R., and Colin Brownlee. "Calcification." In The Physiology of Microalgae, 301–18. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24945-2_14.

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Reitner, Joachim, and Volker Thiel. "Calcification." In Encyclopedia of Geobiology, 211. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-1-4020-9212-1_235.

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Yudin, Andrey. "Popcorn Calcification, Target Calcification, and Bull’s Eye Calcification." In Metaphorical Signs in Computed Tomography of Chest and Abdomen, 45. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24494-0_23.

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Moawad, Magdy R. "Management of Peripheral Arterial Calcification." In Cardiovascular Calcification, 205–35. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_11.

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Jashari, Fisnik, Per Wester, and Michael Henein. "Arterial Calcification and Cerebral Disease: Stroke and Dementia." In Cardiovascular Calcification, 237–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_12.

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Mirsadraee, Saeed, and John Pepper. "Calcification and Aortic Syndromes." In Cardiovascular Calcification, 65–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_5.

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Procaccini, Luca, Marzia Olivieri, Francesco Lorenzo Serafini, Cesare Mantini, Erica Maffei, and Filippo Cademartiri. "Imaging Peripheral Arterial Calcifications." In Cardiovascular Calcification, 177–204. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_10.

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Engvall, Jan. "Value of Coronary Calcium-Screening for Risk Assessment in the General Population." In Cardiovascular Calcification, 111–18. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_7.

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Henein, Michael, George Koulaouzidis, and Pompilio Faggiano. "Heart Valve Calcification." In Cardiovascular Calcification, 33–44. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_3.

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Rezvanizadeh, Vahid, and Matthew J. Budoff. "Prognostic Value of Coronary Artery Calcium." In Cardiovascular Calcification, 95–110. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_6.

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Conference papers on the topic "Calcification"

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Yu, Yinshi, Yahui Zhu, Chao Zuo, and Haigang Ma. "Monitoring of microvascular calcification by time-resolved photoacoustic microscopy." In Advanced Optical Imaging Technologies VII, edited by P. Scott Carney, Xiao-Cong Yuan, and Kebin Shi, 30. SPIE, 2024. http://dx.doi.org/10.1117/12.3036394.

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Ferreira, Marcos Venâncio Araújo, Rafael Henrique Neves Gomes, Fabiana Carla dos Santos Correia, Mariana Beber Chamon, Sérgio Roberto Pereira da Silva Júnior, Isadora Chain Lima, Marcus Vinicius de Sousa, Murilo Justino de Almeida, Daniel Sabino de Oliveira, and Thiago Cardoso Vale. "Idiopathic basal ganglia calcification and Hoarding disorder." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.499.

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Introduction: Basal ganglia calcifications are associated with many neurological and metabolic disorders, being present also on asymptomatic patients. It may present in its primary form, including familial and sporadic cases. Its secondary form is associated especially to hypoparathyroidism but also associated to infections, toxic exposure, rheumatologic diseases, mitochondrial disorders. It has an heterogenous clinical presentation with movement disorders and neuropsychiatric symptoms. Case presentation: A 66-year-old patient presented with a progressive hoarding disorder for the last six years. In the last 2 years started an aggressive behavior, loss of acquired skills, urinary incontinence, sleep-wake cicle disorder and one episode of focal seizure. Physical examination revealed bilateral asymmetrical tremor, bradykinesia and cogwheel rigidity. MoCA test was 23/30 for 12 years of schooling. Brain Computed Tomography showed calcifications in basal ganglia affecting predominantly pallidum e thalamus and cerebellar hemispheres. Brain Magnetic Resonance Imaging revealed hypointensites in the same regions and in nucleus caudate suggestive of calcification. Laboratory testing for endocrine and calcium metabolism was normal. No clinical signs of other disorders. Discussion: We presented a case of probable Idiopathic Basal Ganglia Calcification initially treated as a hoarding disorder. The normal laboratory results, lack of other clinical signs and familial history suggests a primary sporadic form that might be due to de novo mutations or transmitted by asymptomatic parent. The most commonly mutations in SLC20A2, PDGFB and PDGFRB but genetic testing is commonly unavailable. Parkinsonism is the most common movement disorder and the neuropsychiatric features include cognitive impairment, psychotic and obsessive compulsive disorders. Conclusion: This case demonstrates that attention is needed to the progression of psychiatric disorders suggesting some rare neurological disorders.
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Patel, Hetal J., and Carlos Girod. "Metastatic Pulmonary Calcification." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2937.

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Zadeh, Parnian Boloori, Hamid N.-Hashemi, Scott C. Corbett, and Ahmet U. Coskun. "Calcification of Trileaflet Polyurethane Heart Valve." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19486.

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Heart valve disease is a common type of cardiac disease that causes a large number of mortalities worldwide. Patients with severe heart valve problems are required to undergo heart valve replacement surgeries. Mechanical and bioprosthetic heart valves are the current available prostheses for patients in need of a heart valve replacement surgery. Mechanical heart valves are susceptible to thromboembolism and thrombosis and bioprosthetic valves have a limited life-span because of leaflet wear and calcification. Different polyurethane valves were suggested as an alternative material. However, prior results indicated that tested polyurethanes failed due to calcification. The mechanism for polyurethane calcification is not yet completely understood. Kou Imachi et al. [2], suggested that the calcification is due to entrapment of blood proteins and/or phospholipids in microgaps in the polymer and subsequent attraction of Ca ion, leading to formation of calcium phosphate (Ca3(PO4)2). Bisphosphonates (BP), which are considered to enhance the calcification resistance of polymers once covalently bonded to the material, indicated promising results in some studies. Focus of the present study is the trileaflet polyurethane valve, originally developed in the design of the AbioCor® replacement heart, and has demonstrated excellent durability and hemocompatibility in clinical evaluation. Over the past three years, this valve has been modified and its potential as a replacement valve have been studied [1]. Valve hemodynamic analysis showed that it is comparable to bioprosthetic valve in terms of fluid flow, pressure drop and regurgitation [1]. In order to ensure the suitability of the trileaflet polyurethane valve as a replacement valve its fatigue and calcification resistance are studied. The purpose of this paper is to simulate calcification of trileaflet polyurethane valves in an in vitro accelerated test and compare that with that of tissue valves. Furthermore the effect of bisphosphonate modified polyurethane on calcification is studied.
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Sarwate, Avneesh. "Calcification and Hybrid Live-Coding." In AM '16: Audio Mostly 2016. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2986416.2986449.

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Mohanalin, J., P. K. Kalra, and Nirmal Kumar. "Fuzzy based micro calcification segmentation." In 2008 International Conference on Electrical and Computer Engineering. IEEE, 2008. http://dx.doi.org/10.1109/icece.2008.4769171.

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de Nooijer, Lennart, Laura Pacho Sampedro, and Gert-Jan Reichart. "The evolution of foraminiferal calcification." In Goldschmidt2021. France: European Association of Geochemistry, 2021. http://dx.doi.org/10.7185/gold2021.4145.

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Al-Enezi, Mamdouh S., Eric Lavallee, Eric Turcotte, Abdelouahed Khalil, Tamas Fulop, Michel Nguyen, and M'hamed Bentourkia. "Assessment of Arterial Wall Calcification with CT and Micro-Calcification with 18F-NaF PET." In 2021 IEEE Nuclear Science Symposium and Medical Imaging Conference (NSS/MIC). IEEE, 2021. http://dx.doi.org/10.1109/nss/mic44867.2021.9875685.

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Carrier, Daniel J. "Flue gas scrubber water de-calcification." In 33rd Biennial Meeting of American Society of Sugarbeet Technologist. ASSBT, 2005. http://dx.doi.org/10.5274/assbt.2005.76.

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Jabłońska, Mariola, and Janusz Janeczek. "Atmospheric Dust-Induced Calcification of Lungs." In Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.1157.

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Reports on the topic "Calcification"

1

Maidment, Andrwe D. A Novel Method for Determining Calcification Composition. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada411733.

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Maidment, Andrew D. A Novel Method for Determining Calcification Composition. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417963.

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Maidment, Andrew D. A Novel Method for Determining Calcification Composition. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada472940.

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Baird, Kaitlin, Anne Cohen, and Samantha de Putron. Ocean Acidification: Building a Skeleton in a Changing Ocean. American Museum of Natural History, 2015. http://dx.doi.org/10.5531/cbc.ncep.0168.

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Coral reefs are particularly vulnerable to ocean acidification due to their calcium carbonate “skeletons,” yet little is known about how ocean acidification will affect coral recruitment. In this exercise, students will examine a species of stony or hard coral belonging to the Order Scleractinia, Favia fragum, and examine how ocean acidification and changes in seawater saturation state (carbonate ion concentration) can affect the calcification process of new recruits of this coral species in Bermuda. After a brief introduction to coral reproduction and recruitment, as well as the chemistry behind calcification and acidification, students will go on to understand the experimental design, obtain and manipulate real data, and analyze the dataset.
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Cushing, Donish, Darshana Goakar, and Bomi Joseph. Higher bioactivity cannabidiol in greater concentration more greatly reduces valvular interstitial cell calcification. Peak Health Center, September 2018. http://dx.doi.org/10.31013/2001f.

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Nikitina, N. V., N. V. Aleksandrova, and A. V. Aleksandrov. Determining the severity of valvular calcification according to echocardiography in patients with rheumatoid arthritis. ООО ИМА-Пресс, 2018. http://dx.doi.org/10.18411/1995-4484-2018-56-3(2)-57.

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Armstrong, Matthew, Jiahong Sun, Feitong Wu, Bo Xi, and Costan Magnussen. The association between youth blood pressure and adult coronary artery calcification: A systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0015.

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Seifert, Miriam, Claudia Hinrichs, Judith Hauck, and Christoph Völker. New / improved model parametrizations for responses in phytoplankton growth and calcification to changes in alkalinity implemented. OceanNets, March 2023. http://dx.doi.org/10.3289/oceannets_d4.5.

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Global biogeochemical ocean models that are currently in place to investigate alkalinity enhancement at a global scale do usually not consider the effects of a changing carbonate system on phytoplankton. We introduce new and modified parameterizations of phytoplankton carbonate systems sensitivities into the biogeochemistry model REcoM. We then compare phytoplankton biomass and net primary production at different atmospheric CO2 concentrations to results from other deliverables (D5.3, 5.6, 5.7) based on experiments and models. The resilience of phytoplankton biomass towards low CO2 concentrations in our model compares well with the results of mesocosm experiments. Or model results differ in the phytoplankton responses compared to the results of a 1D biogeochemical model that employs similar parameterizations regarding the effects on calcifying phytoplankton and total net primary production, which we explain primarily with differences in the spatial scales and phytoplankton communities investigated.
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Sheng, Chang, Weihua Huang, Mingmei Liao, and Pu Yang. Association of the Abdominal Aortic Calcification with All-Cause and Cardiovascular Disease-Specific Mortality: Prospective Cohort Study. World Journal of Surgery, April 2024. http://dx.doi.org/10.60123/j.wjs.2024.10.03.

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Background: Abdominal aortic calcification (AAC) is a prevalent form of vascular calcification associated with adverse cardiovascular outcomes. While previous studies on AAC and cardiovascular risk exist, many have limitations such as small sample sizes and limited clinical significance outcomes. This study aims to prospectively investigate the association between AAC and all-cause and cardiovascular disease (CVD)-specific mortality rates in a nationally representative sample of adults in the United States, using data from the National Health and Nutrition Examination Survey (NHANES). Methods: The study, conducted on NHANES participants aged 40 years or older during the 2013-2014 cycle, assessed AAC using the Kauppila scoring system. Demographic characteristics, mortality data, and comorbid factors such as age, gender, diabetes, and hypertension were considered. Statistical analyses, including weighted percentages, Kaplan-Meier survival curves, and multivariable Cox proportional hazards regression models, were employed to evaluate the associations between AAC and mortality risks. Results: After analyzing a final sample of 2717 participants, the study found a significant association between severe AAC (SAAC) and higher all-cause mortality risk (HR 1.70, 95% CI 1.17-2.48). The dose-response relationship indicated an increased risk with higher AAC scores. However, no independent association was observed between AAC and cardiovascular mortality. Stratified analysis revealed variations in the AAC-all-cause mortality association based on gender and hypertension. Conclusion: This population-based study provides valuable insights into the prospective association between AAC and all-cause mortality, emphasizing the potential role of AAC assessment in identifying individuals at higher risk.
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Cushing, Donish, Darshana Goakar, and Bomi Joseph. Bioactive cannabidiol more greatly reduces valvular interstitial cell calcification when combined with ß-Caryophyllene, and α-Humulene. Peak Health Center, September 2018. http://dx.doi.org/10.31013/2001g.

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