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1
Rutsch, Frank, and Robert Terkeltaub. "Deficiencies of physiologic calcification inhibitors and low-grade inflammation in arterial calcification: lessons for cartilage calcification." Joint Bone Spine 72, no. 2 (March 2005): 110–18. http://dx.doi.org/10.1016/j.jbspin.2004.05.014.
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Herrmann, Jaqueline, Milen Babic, Markus Tölle, Markus van der Giet, and Mirjam Schuchardt. "Research Models for Studying Vascular Calcification." International Journal of Molecular Sciences 21, no. 6 (March 23, 2020): 2204. http://dx.doi.org/10.3390/ijms21062204.
Повний текст джерелаАнотація:
Calcification of the vessel wall contributes to high cardiovascular morbidity and mortality. Vascular calcification (VC) is a systemic disease with multifaceted contributing and inhibiting factors in an actively regulated process. The exact underlying mechanisms are not fully elucidated and reliable treatment options are lacking. Due to the complex pathophysiology, various research models exist evaluating different aspects of VC. This review aims to give an overview of the cell and animal models used so far to study the molecular processes of VC. Here, in vitro cell culture models of different origins, ex vivo settings using aortic tissue and various in vivo disease-induced animal models are summarized. They reflect different aspects and depict the (patho)physiologic mechanisms within the VC process.
3
Scott, J. E., and M. Haigh. "Is dermatan sulfate proteoglycan the physiologic inhibitor of type I collagen calcification?" Bone 7, no. 2 (January 1986): 154. http://dx.doi.org/10.1016/8756-3282(86)90717-9.
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4
Doyle, Anthony James, and Graeme D. Anderson. "Physiologic Calcification of the Pineal Gland in Children on Computed Tomography: Prevalence, Observer Reliability and Association with Choroid Plexus Calcification." Academic Radiology 13, no. 7 (July 2006): 822–26. http://dx.doi.org/10.1016/j.acra.2006.04.004.
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5
Al-Zaghal, Abdullah, Siavash Mehdizadeh Seraj, Thomas J. Werner, Oke Gerke, Poul F. Høilund-Carlsen, and Abass Alavi. "Assessment of Physiologic Intracranial Calcification in Healthy Adults Using 18F-NaF PET/CT." Journal of Nuclear Medicine 60, no. 2 (July 12, 2018): 267–71. http://dx.doi.org/10.2967/jnumed.118.213678.
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6
Caliskan, Emine, and Mehmet Ozturk. "Evaluation of physiologic pineal gland calcification via computed tomography in the pediatric population." Annals of Medical Research 26, no. 10 (2019): 2391. http://dx.doi.org/10.5455/annalsmedres.2019.06.338.
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Nemes, Attila, and Tamás Forster. "Functional vascular alterations associated with aortic valve stenosis." Orvosi Hetilap 152, no. 25 (June 2011): 993–99. http://dx.doi.org/10.1556/oh.2011.29145.
Повний текст джерелаАнотація:
Degenerative changes, atherosclerotic process and calcification of valvular leaflets are mostly responsible for valvular aortic valve stenosis, but congenital bicuspid aortic valve and rheumatic fever in history are also known predisposing factors. Aortic valve stenosis is frequently associated with different functional vascular alterations. The aim of this review is to demonstrate these vascular alterations evaluated by non-invasive methods and underlying physiologic and pathophysiologic processes. Orv. Hetil., 2011, 152,993–999.
8
Rezvova, M. A., E. A. Ovcharenko, T. V. Glushkova, Yu A. Kudryavtseva, and L. S. Barbarash. "Evaluation of calcification resistance of xenopericardium treated with polyhydroxy compounds." Russian Journal of Transplantology and Artificial Organs 23, no. 1 (April 10, 2021): 75–83. http://dx.doi.org/10.15825/1995-1191-2021-1-75-83.
Повний текст джерелаАнотація:
Calcification of biomaterials used in prosthetic heart valves has been a challenging issue in cardiovascular surgery. The objective of this work is to compare the efficiency of polyvinyl alcohol (PVA) and tannic acid (TA) modification of xenomaterials, pre-stabilized with glutaraldehyde (GA) and ethylene glycol diglycidyl ether (EGDE), in reducing calcification. Analysis of mechanical properties evaluated under uniaxial tension, showed a significant increase in the tensile strength of the test samples compared to the control (unmodified) samples (p < 0.05). Additional treatment of GA-fixed tissue with PVA and TA significantly reduced the amount of calcium in the samples implanted into rats for a 60-day follow-up (p < 0.05). The level of calcification of samples prestabilized with EGDE and treated with PVA and TA did not differ from the control group (p = 0.063). Cumulative analysis of the study results demonstrated that the GA-fixed biomaterial modified with PVA and TA can reduce calcium-binding activity and increase strength. This indicates the prospects for clinical application of the proposed treatment methods. This being said, the issue of long-term body response requires further study of the long-term stability of the modified biomaterial under physiologic blood flow conditions.
9
Fukai, Atsushi, Naohiro Kawamura, Taku Saito, Yasushi Oshima, Toshiyuki Ikeda, Fumitaka Kugimiya, Akiro Higashikawa, et al. "Akt1 in murine chondrocytes controls cartilage calcification during endochondral ossification under physiologic and pathologic conditions." Arthritis & Rheumatism 62, no. 3 (February 25, 2010): 826–36. http://dx.doi.org/10.1002/art.27296.
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Terkeltaub, Robert. "Physiologic and pathologic functions of the NPP nucleotide pyrophosphatase/phosphodiesterase family focusing on NPP1 in calcification." Purinergic Signalling 2, no. 2 (June 2006): 371–77. http://dx.doi.org/10.1007/s11302-005-5304-3.
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11
Pasch, Andreas, Willi Jahnen-Dechent, and Edward R. Smith. "Phosphate, Calcification in Blood, and Mineral Stress: The Physiologic Blood Mineral Buffering System and Its Association with Cardiovascular Risk." International Journal of Nephrology 2018 (September 2, 2018): 1–5. http://dx.doi.org/10.1155/2018/9182078.
Повний текст джерелаАнотація:
Phosphate is an important cardiovascular risk factor and lowering elevated blood phosphate concentrations is a main therapeutic target in kidney patients. Phosphate is subject to the blood mineral buffering system which controls the precipitation of calcium and phosphate. Calciprotein particles (CPP), self-assembling complexes of calcium phosphate and serum proteins, are the nanomorphological correlates of this system. CPP1 are spherical, 50-100 nm in diameter, and contain amorphous mineral. CPP2 are oblongated, 100-200nm in the long axis, and they contain a crystalline mineral core. The relative abundance and biological activity of these particles are a matter of intense research, because they can cause oxidative stress, inflammation, and calcification in cellular assay. Therapeutically reducing this endogenous stressor by prolonging crystal formation time might improve patient outcome. This concise review article summarizes our current knowledge about the blood mineral buffering system and proposes Mineral Stress as a novel modifiable cardiovascular risk factor. It furthermore outlines possible implications this might have for improving patient care.
12
Som, Panchali, Rajarshi Roy, Sumit Datta, Asis Kumar Ghosal, Anubha Saha, and Subhajit Halder. "Physiological Intracranial Calcification in Eastern Indian Population-A CT Scan Study." National Journal of Clinical Anatomy 06, no. 01 (January 2017): 059–70. http://dx.doi.org/10.1055/s-0039-1700723.
Повний текст джерелаАнотація:
Abstract Background and Aims:Knowledge of physiological calcification in brain parenchyma is essential to avoid misinterpretation during radiological evaluation. The calcifications are commonly seen in pineal gland, falx cerebri, tentorium cerebelli and choroid plexus. Objective:To determine the incidence of physiological intracranial calcification and its relationship to age and sex in eastern Indian population. Materials and Method: A cross sectional descriptive study of CT scan brain was performed in age group between 20-80 yrs in eastern India. The study was conducted on 64 Slice MDCT PHILIPS Brilliance. Bulk of our patients was of road traffic accidents and routine CT scan study revealed these physiological calcifications and did not possess any morphological abnormality. Results: 852 patients of which 503 male and 349 female were studied and overall 1429 separate calcified areas were identified due to co-existent calcifications in most of the patients. The incidence of calcification was in pineal gland (62%), choroid plexus (53%), dura mater (26%), basal ganglia (2.8%), dentate nucleus (1.4%) and Habenular nuclei (6%). Incidence is more in male than in female. Conclusion: Physiological calcifications in some of the intracranial structures are not a very uncommon finding and it should not be confused with a pathological one.
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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.
Повний текст джерелаАнотація:
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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Scissons, Robert P., Abraham Ettaher, and Sophia Afridi. "Likelihood of Normal ABI Increases With Physiologic Testing Referrals From Rural Primary Care Physicians." Journal for Vascular Ultrasound 43, no. 3 (August 29, 2019): 123–27. http://dx.doi.org/10.1177/1544316719870070.
Повний текст джерелаАнотація:
Disparities in diagnostic capabilities have been noted between rural and urban health care facilities. We believe the clinical evaluation of peripheral arterial disease (PAD) by rural physicians may be similarly affected. Patients referred for arterial physiologic testing in an urban and rural regional health care network for a consecutive 7-month period were reviewed. Patients were classified into 3 groups based on referring physician specialty: (1) vascular surgeon or vascular medicine specialist (Vasc), (2) urban primary care physician (Urban), and (3) rural primary care physician (Rural). Normal patients were defined by a posterior tibial (PT) or dorsalis pedis (DP) ankle-brachial index (ABI) of ⩾0.90, bilaterally. Abnormal patients had both PT and DP ABI <0.90 in one or both extremities. Group comparisons were made for normal and abnormal patients, age (⩾65 years old), and gender. Patients with history of amputations, angioplasty, bypass graft, stent, calcification (PT or DP ABI ⩾1.30), and previous physiologic testing outside the designated period of analysis were considered a separate subclassification and analyzed separately. Emergency room referrals, inpatients, and patients with incomplete examination data were excluded from the analysis. A total of 430 patient exams were evaluated. Group-Rural had significantly greater numbers of normal ABI patients compared with Group-Urban ( P = .0028) and Group-Vasc ( P = .0000). No significant differences were noted between all groups for age and gender. Substantial disparities were noted in normal and abnormal ABI patients between rural health care physicians and their urban primary care and vascular specialist counterparts. Significantly greater numbers of normal ABI referrals by rural primary care physicians may warrant enhanced PAD diagnosis education or telemedicine alternatives.
15
Olesen, Ping, Kirsten Nguyen, Lise Wogensen, Thomas Ledet, and Lars Melholt Rasmussen. "Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 2 (February 2007): H1058—H1064. http://dx.doi.org/10.1152/ajpheart.00047.2006.
Повний текст джерелаАнотація:
Arterial medial calcifications occur often in diabetic individuals as part of the diabetic macroangiopathy. The pathogenesis is unknown, but the presence of calcifications predicts risk of cardiovascular events. We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). Human vascular smooth muscle cells (VSMCs) were grown from aorta from kidney donors. Induction of calcification was performed with β-glycerophosphate. The influence of insulin (200 μU/ml or 1,000 μU/ml) on calcification was judged by measuring calcium content in the cell layer and by von Kossa staining. OPG was measured in the medium by ELISA. Histochemistry was used for determination of alkaline phosphatase (ALP). Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. β-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. Decreased OPG amounts were observed from the cells during the accelerated calcification phase. High dose of insulin (1,000 μU/ml) accelerated the calcification, whereas lower concentrations (200 μU/ml) did not. Calcified cells expressed ALP and BSP activity in high levels. In conclusion, high concentration of insulin enhances in vitro-induced calcification in VSMCs. Altered OPG levels during the calcification raise the possibility that OPG may have a potent function in regulating the calcification process or it may represent a consequence of mineralization. Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy.
16
Beattie, D., C. Xu, R. Vito, S. Glagov, and M. C. Whang. "Mechanical Analysis of Heterogeneous, Atherosclerotic Human Aorta." Journal of Biomechanical Engineering 120, no. 5 (October 1, 1998): 602–7. http://dx.doi.org/10.1115/1.2834750.
Повний текст джерелаАнотація:
An experimental technique was developed to determine the finite strain field in heterogeneous, diseased human aortic cross sections at physiologic pressures in vitro. Also, the distributions within the cross sections of four histologic features (disease-free zones, lipid accumulations, fibrous intimal tissue, and regions of calcification) were quantified using light microscopic morphometry. A model incorporating heterogeneous, plane stress finite elements coupled the experimental and histologic data. Tissue constituent mechanical properties were determined through an optimization strategy, and the distributions of stress and strain energy in the diseased vascular wall were calculated. Results show that the constituents of atherosclerotic lesions exhibit large differences in their bilinear mechanical properties. The distributions of stress and strain energy in the diseased vascular wall are strongly influenced by both lesion structure and composition. These results suggest that accounting for heterogeneities in the mechanical analysis of atherosclerotic arterial tissue is critical to establishing links between lesion morphology and the susceptibility of plaque to mechanical disruption in vivo.
17
Friedland, Robert P., Jay S. Luxenberg, and Elisabeth Koss. "A Quantitative Study of Intracranial Calcification in Dementia of the Alzheimer Type." International Psychogeriatrics 2, no. 1 (March 1990): 37–43. http://dx.doi.org/10.1017/s104161029000028x.
Повний текст джерелаАнотація:
Abnormalities in calcium homeostasis have been reported in Alzheimer's disease (AD) and in the neurofibrillary tangle disorders of amyotrophic lateral sclerosis and parkinsonism-dementia occurring in the Pacific. In order to more fully evaluate calcium physiology in AD, we analyzed the size of pineal and choroid plexus calcifications, using X-ray computed tomography, in 23 patients with probable AD and 18 healthy age-matched control subjects. The area occupied by calcification was measured from hard copies of the data by two independent observers who were blind to the diagnosis. There were no differences in the areas occupied by pineal or choroid plexus calcifications between the two groups. These data suggest that AD is not accompanied by alternations in intracranial calcium deposition in pineal gland or choroid plexus.
18
Bazin, Dominique, Arnaud Dessombz, Christelle Nguyen, Hang Korng Ea, Frédéric Lioté, John Rehr, Christine Chappard, et al. "The status of strontium in biological apatites: an XANES/EXAFS investigation." Journal of Synchrotron Radiation 21, no. 1 (November 2, 2013): 136–42. http://dx.doi.org/10.1107/s1600577513023771.
Повний текст джерелаАнотація:
Osteoporosis represents a major public health problem through its association with fragility fractures. The public health burden of osteoporotic fractures will rise in future generations, due in part to an increase in life expectancy. Strontium-based drugs have been shown to increase bone mass in postmenopausal osteoporosis patients and to reduce fracture risk but the molecular mechanisms of the action of these Sr-based drugs are not totally elucidated. The local environment of Sr2+cations in biological apatites present in pathological and physiological calcifications in patients without such Sr-based drugs has been assessed. In this investigation, X-ray absorption spectra have been collected for 17 pathological and physiological calcifications. These experimental data have been combined with a set of numerical simulations using theab initioFEFF9X-ray spectroscopy program which takes into account possible distortion and Ca/Sr substitution in the environment of the Sr2+cations. For selected samples, Fourier transforms of the EXAFS modulations have been performed. The complete set of experimental data collected on 17 samples indicates that there is no relationship between the nature of the calcification (physiological and pathological) and the adsorption mode of Sr2+cations (simple adsorption or insertion). Such structural considerations have medical implications. Pathological and physiological calcifications correspond to two very different preparation procedures but are associated with the same localization of Sr2+versusapatite crystals. Based on this study, it seems that for supplementation of Sr at low concentration, Sr2+cations will be localized into the apatite network.
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Bäck, Magnus, and Jean-Baptiste Michel. "From organic and inorganic phosphates to valvular and vascular calcifications." Cardiovascular Research 117, no. 9 (February 9, 2021): 2016–29. http://dx.doi.org/10.1093/cvr/cvab038.
Повний текст джерелаАнотація:
Abstract Calcification of the arterial wall and valves is an important part of the pathophysiological process of peripheral and coronary atherosclerosis, aortic stenosis, ageing, diabetes, and chronic kidney disease. This review aims to better understand how extracellular phosphates and their ability to be retained as calcium phosphates on the extracellular matrix initiate the mineralization process of arteries and valves. In this context, the physiological process of bone mineralization remains a human model for pathological soft tissue mineralization. Soluble (ionized) calcium precipitation occurs on extracellular phosphates; either with inorganic or on exposed organic phosphates. Organic phosphates are classified as either structural (phospholipids, nucleic acids) or energetic (corresponding to phosphoryl transfer activities). Extracellular phosphates promote a phenotypic shift in vascular smooth muscle and valvular interstitial cells towards an osteoblast gene expression pattern, which provokes the active phase of mineralization. A line of defense systems protects arterial and valvular tissue calcifications. Given the major roles of phosphate in soft tissue calcification, phosphate mimetics, and/or prevention of phosphate dissipation represent novel potential therapeutic approaches for arterial and valvular calcification.
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Bazin, D., M. Daudon, Ch Chappard, J. J. Rehr, D. Thiaudière, and S. Reguer. "The status of strontium in biological apatites: an XANES investigation." Journal of Synchrotron Radiation 18, no. 6 (September 16, 2011): 912–18. http://dx.doi.org/10.1107/s0909049511032651.
Повний текст джерелаАнотація:
Osteoporosis represents a major public health problem and increases patient morbidity through its association with fragility fractures. Among the different treatments proposed, strontium-based drugs have been shown to increase bone mass in postmenopausal osteoporosis patients and to reduce fracture risk. While the localization of Sr2+cations in the bone matrix has been extensively studied, little is known regarding the status of Sr2+cations in natural biological apatite. In this investigation the local environment of Sr2+cations has been investigated through XANES (X-ray absorption near-edge structure) spectroscopy in a set of pathological and physiological apatites. To assess the localization of Sr2+cations in these biological apatites, numerical simulations using theab initioFEFF9X-ray spectroscopy program have been performed. The complete set of data show that the XANES part of the absorption spectra may be used as a fingerprint to determine the localization of Sr2+cationsversusthe mineral part of calcifications. More precisely, it appears that a relationship exists between some features present in the XANES part and a Sr2+/Ca2+substitution process in site (I) of crystal apatite. Regarding the data, further experiments are needed to confirm a possible link between the relationship between the preparation mode of the calcification (cellular activity for physiological calcification and precipitation for the pathological one) and the adsorption mode of Sr2+cations (simple adsorption or insertion). Is it possible to draw a line between life and chemistry through the localization of Sr in apatite? The question is open for discussion. A better structural description of these physiological and pathological calcifications will help to develop specific therapies targeting the demineralization process in the case of osteoporosis.
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De Maré, Annelies, Stuart Maudsley, Abdelkrim Azmi, Jhana O. Hendrickx, Britt Opdebeeck, Ellen Neven, Patrick C. D’Haese, and Anja Verhulst. "Sclerostin as Regulatory Molecule in Vascular Media Calcification and the Bone–Vascular Axis." Toxins 11, no. 7 (July 21, 2019): 428. http://dx.doi.org/10.3390/toxins11070428.
Повний текст джерелаАнотація:
Sclerostin is a well-known inhibitor of bone formation that acts on Wnt/β-catenin signaling. This manuscript considers the possible role of sclerostin in vascular calcification, a process that shares many similarities with physiological bone formation. Rats were exposed to a warfarin-containing diet to induce vascular calcification. Vascular smooth muscle cell transdifferentiation, vascular calcification grade, and bone histomorphometry were examined. The presence and/or production of sclerostin was investigated in serum, aorta, and bone. Calcified human aortas were investigated to substantiate clinical relevance. Warfarin-exposed rats developed vascular calcifications in a time-dependent manner which went along with a progressive increase in serum sclerostin levels. Both osteogenic and adipogenic pathways were upregulated in calcifying vascular smooth muscle cells, as well as sclerostin mRNA and protein levels. Evidence for the local vascular action of sclerostin was found both in human and rat calcified aortas. Warfarin exposure led to a mildly decreased bone and mineralized areas. Osseous sclerostin production and bone turnover did not change significantly. This study showed local production of sclerostin in calcified vessels, which may indicate a negative feedback mechanism to prevent further calcification. Furthermore, increased levels of serum sclerostin, probably originating from excessive local production in calcified vessels, may contribute to the linkage between vascular pathology and impaired bone mineralization.
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Kolotilov, Nikolay. "Pineal gland calcifications in patients with benign and malignant tumors of the larynx, pharynx, paranasal sinuses and auditory nerve." Radiation Diagnostics, Radiation Therapy, no. 2 (2020): 18–27. http://dx.doi.org/10.37336/2707-0700-2020-2-2.
Повний текст джерелаАнотація:
Calcifications of the brain – pineal gland, choroid plexuses of the lateral ventricles – are a long-known phenomenon. Calcification in such functionally important organs as the pineal gland and choroid plexuses of the lateral ventricles cannot be physiological (it is enough to recall the formation of stones in the gallbladder, kidneys, prostate gland, calcinosis of the heart valves and coronary vessels) or relatively neutral process in the body and not affect the activity of these organs. The purpose of the investigation is to study the nosological predisposition of calcifications and the incidence of calcification of the pineal gland and choroid plexuses of the lateral ventricles in benign and malignant tumors of the larynx, pharynx, paranasal sinuses and auditory nerve. Material and research methods. The analysis of CT images of 425 persons was carried out (data archive of the Institute): 50 practically healthy persons from 22 to 60 years without any chronic diseases of the head and neck and a history of surgical interventions; 23 – from 61 to 74 years with normal body aging, not taking any medications, with healthy lifestyle; 235 – from 22 to 74 years with maxillary sinus cysts; 61 – from 28 to 71 years with acoustic neuromas; 56 – from 14 to 74 years with benign and malignant tumors of the larynx, nasal pharynx and paranasal sinuses. Conclusions. Pineal gland calcifications – can be considered as: mobile depot or cemetery of calcium; the result of an organ and/or a tumor-bearing organism protective reaction; a sign of a normal or decreased pineal gland function. The formation and growth of calcifications of the pineal gland and choroid plexuses of the lateral ventricles is associated with the growth and development of the body, benign and malignant tumors of the larynx, pharynx, paranasal sinuses and the auditory nerve (very likely, the tumors of other localizations as well). The formation and growth of calcifications of the pineal gland and choroid plexuses of the lateral ventricles indicates an increase of the heterogeneity of the human body tissues and organs with age and the acquisition of diseases.
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Harpa, Marius Mihai, Ionela Movileanu, Leslie Neil Sierad, Ovidiu Simion Cotoi, Horatiu Suciu, Carmen Sircuta, Terezia Preda, et al. "Pulmonary heart valve replacement using stabilized acellular xenogeneic scaffolds; effects of seeding with autologous stem cells." Revista Romana de Medicina de Laborator 23, no. 4 (December 1, 2015): 415–30. http://dx.doi.org/10.1515/rrlm-2015-0046.
Повний текст джерелаАнотація:
Abstract Background: We hypothesized that an ideal heart valve replacement would be acellular valve root scaffolds seeded with autologous stem cells. To test this hypothesis, we prepared porcine acellular pulmonary valves, seeded them with autologous adipose derived stem cells (ADSCs) and implanted them in sheep and compared them to acellular valves. Methods: Fresh porcine pulmonary valve roots were decellularized with detergents and enzymes. ADSCs were isolated from subdermal fat and injected within the acellular cusps. Valves were then implanted in an extra-anatomic pulmonary position as RV to PA shunts: Group A (n=6) consisted of acellular valves and Group B (n=6) of autologous stem cell-seeded acellular xenografts. Sheep were followed up for 6 months by echocardiography and histologic analysis was performed on explanted valves. Results: Early evolution was favorable for both groups. All Group A animals had physiologic growth without any signs of heart failure and leaflets were found with preserved structure and mobility, lacking signs of thrombi, inflammation or calcification. Group B sheep however expressed signs of right ventricle failure starting at one month, accompanied by progressive regurgitation and right ventricle dilatation, and the leaflets were found covered with host tissue. No cells were found in any Group A or B explants. Conclusions: Acellular stabilized xenogeneic pulmonary valves are reliable, stable, non-immunogenic, non-thrombogenic and non-calcifying scaffolds with excellent hemodynamics. Seeding these scaffolds with autologous ADSCs was not conducive to tissue regeneration. Studies aimed at understanding these novel observations and further harnessing the potential of stem cells are ongoing.
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Witteman, Jacqueline CM. "Coronary calcification detected by electron-beam computed tomography and non-coronary measures of atherosclerosis:." Circulation 103, suppl_1 (March 2001): 1344. http://dx.doi.org/10.1161/circ.103.suppl_1.9999-4.
Повний текст джерелаАнотація:
0004 Coronary calcification as detected by electron-beam tomography (EBT) is a measure of coronary atherosclerosis. We investigated whether coronary artery calcium is associated with non-coronary measures of atherosclerosis, using data from the population-based Rotterdam Study. Participants in the third phase of the study were invited to undergo EBT scanning for detection of coronary calcifications. EBT scans were obtained from 2263 participants (47% men, mean age (SD), 71.3 (5.7)). Quantification of coronary calcifications was performed using Agatston’s method, and resulted in a calcium score. Calcium scores were available for 1874 subjects. Measures of non-coronary atherosclerosis included presence of aorta calcification detected by X-ray, presence of plaques in carotid arteries and intima-media thickness of the common carotid artery, both detected by ultrasonography, and ankle to brachial blood pressure index as a measure of peripheral arterial disease. Three calcium score categories were considered: 0 - 100, 101 - 500, and >500. The calcium score showed a graded association with the measures of non-coronary atherosclerosis. Using logistic regression analysis, age and sex adjusted odds ratios for aorta calcification were 3.2 (95% confidence interval, 2.0 - 5.2) in subjects with calcium score 101 - 500 and 12.0 (7.6 - 18.9) in subjects with calcium score > 500, when compared to subjects in the lowest calcium score category. The corresponding odds ratios for carotid plaques were 2.4 (1.6 - 3.5) and 5.8 (3.9 - 8.6). In a general linear model adjusted for age and sex, mean intima-media thickness increased with increasing calcium score category, while mean ankle to brachial blood pressure index decreased. These results indicate that known measures of non-coronary atherosclerosis are strongly related to coronary atherosclerosis, as measured by EBT calcium.
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Schinzari, Francesca, Manfredi Tesauro, Aldo Bertoli, Alessia Valentini, Augusto Veneziani, Umberto Campia, and Carmine Cardillo. "Calcification biomarkers and vascular dysfunction in obesity and type 2 diabetes: influence of oral hypoglycemic agents." American Journal of Physiology-Endocrinology and Metabolism 317, no. 4 (October 1, 2019): E658—E666. http://dx.doi.org/10.1152/ajpendo.00204.2019.
Повний текст джерелаАнотація:
Vascular aging in obesity and type 2 diabetes (T2D) is associated with progressive vascular calcification, an independent predictor of morbidity and mortality. Pathways for vascular calcification modulate bone matrix deposition, thus regulating calcium deposits. We investigated the association between biomarkers of vascular calcification and vasodilator function in obesity or T2D, and whether antidiabetic therapies favorably impact those markers. Circulating levels of proteins involved in vascular calcification, such as osteopontin (OPN), osteoprotegerin (OPG), regulated on activation, normal T cell expressed and secreted (RANTES), and fetuin-A were measured in lean subjects, individuals with metabolically healthy obesity (MHO), and patients with metabolically unhealthy obesity (MUO) or T2D. Vasodilator function was assessed by infusion of ACh and sodium nitroprusside (SNP). Circulating levels of OPN were higher in the MUO/T2D group than in lean subjects ( P < 0.05); OPG and RANTES were higher in MUO/T2D group than in the other groups (both P < 0.001); fetuin-A was not different between groups ( P > 0.05); vasodilator responses to either ACh or SNP were impaired in both MUO/T2D and MHO compared with lean subjects (all P < 0.001). In patients with T2D who were enrolled in the intervention trial, antidiabetic treatment with glyburide, metformin, or pioglitazone resulted in a significant reduction of circulating OPG ( P = 0.001), without changes in the other biomarkers and vasodilator responses (all P > 0.05). In conclusion, obese patients with MUO/T2D have elevated circulating OPN, OPG, and RANTES; in these patients, antidiabetic treatment reduces only circulating OPG. Further study is needed to better understand the mechanisms of vascular calcifications in obesity and diabetes.
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Tong, Wenjuan, Xiaoling Zhang, Jia Luo, Fushun Pan, Jinyu Liang, Hui Huang, Manying Li, et al. "Value of multimodality imaging in the diagnosis of breast lesions with calcification: A retrospective study." Clinical Hemorheology and Microcirculation 76, no. 1 (October 15, 2020): 85–98. http://dx.doi.org/10.3233/ch-200877.
Повний текст джерелаАнотація:
PURPOSE: To assess the value of conventional ultrasound (US), contrast-enhanced ultrasound (CEUS) and mammography in the diagnosis of breast lesions with calcifications. METHODS: A total of 87 breast lesions with calcification were subjected to US, CEUS and mammography and divided into 3 groups: Group A (all cases), Group A1 (31 cases who underwent US and CEUS first followed by mammography), and Group A2 (56 cases who underwent mammography first followed by US and CEUS). A receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic efficacy of different methods in different groups. RESULTS: In Group A, the area under the ROC curve (AUROC) of CEUS were 0.937, which were significantly higher than that of mammography (p < 0.05). In Group A1, the AUROC of CEUS were 0.842, which were not significantly different from that of US and mammography (p > 0.05). In Group A2, the AUROC of CEUS were 0.987, which were significantly higher than that of mammography and US (p < 0.05). CONCLUSION: Based on the mammography results, the combination of US and CEUS might improve the diagnostic efficacy in breast lesions with calcification.
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Ross, Claire L., Verena Schoepf, Thomas M. DeCarlo, and Malcolm T. McCulloch. "Mechanisms and seasonal drivers of calcification in the temperate coral Turbinaria reniformis at its latitudinal limits." Proceedings of the Royal Society B: Biological Sciences 285, no. 1879 (May 23, 2018): 20180215. http://dx.doi.org/10.1098/rspb.2018.0215.
Повний текст джерелаАнотація:
High-latitude coral reefs provide natural laboratories for investigating the mechanisms and limits of coral calcification. While the calcification processes of tropical corals have been studied intensively, little is known about how their temperate counterparts grow under much lower temperature and light conditions. Here, we report the results of a long-term (2-year) study of seasonal changes in calcification rates, photo-physiology and calcifying fluid (cf) chemistry (using boron isotope systematics and Raman spectroscopy) for the coral Turbinaria reniformis growing near its latitudinal limits (34.5° S) along the southern coast of Western Australia. In contrast with tropical corals, calcification rates were found to be threefold higher during winter (16 to 17° C) compared with summer (approx. 21° C), and negatively correlated with light, but lacking any correlation with temperature. These unexpected findings are attributed to a combination of higher chlorophyll a, and hence increased heterotrophy during winter compared with summer, together with the corals' ability to seasonally modulate pH cf , with carbonate ion concentration being the main controller of calcification rates. Conversely, calcium ion concentration [Ca 2+ ] cf declined with increasing calcification rates, resulting in aragonite saturation states Ω cf that were stable yet elevated fourfold above seawater values. Our results show that corals growing near their latitudinal limits exert strong physiological control over their cf in order to maintain year-round calcification rates that are insensitive to the unfavourable temperature regimes typical of high-latitude reefs.
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Zare, Ahmad, and Sara Choudhry. "Bilateral Basal Ganglia Calcification; An Unusual Initial Presentation of Pseudohypoparathyroidism." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A184—A185. http://dx.doi.org/10.1210/jendso/bvab048.373.
Повний текст джерелаАнотація:
Abstract Physiological intracranial calcification occurs in about 0.3–1.5% of cases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. A 21-year-old female who was initially evaluated by neurology team for headache and diplopia, underwent MRI of brain which revealed Calcifications involving the bilateral basal ganglia, thalami, dentate nuclei as well as juxtacortical frontal lobes. She reported Fatigue and muscle pain, usually in her arms especially after playing sports which had been going on for many years. She had no history of fractures, seizures, psychiatric disorders, developmental delay or obvious cognitive impairments. She denied any family history of calcium disorders or autoimmune diseases. As she had been generally healthy in her whole life, she never had any lab testing done. On examination, Height 5’1”, Chvostek’s sign was positive. Fundoscopy was normal. she had no dysmorphic features or shortened 4th metacarpal. Investigations revealed serum calcium less than 5.0 mg (N 8.3 - 10.1 mg/dl), PTH 205.1 pg/ml (N 18.4 - 80.1 pg/ml), phosphate 7.1 mg (N 2.5 - 5 mg), Vitamin-D 36.2 ng/ml (N 30.0 - 100.0 pg/ml),magnesium 2.0 m (N 1.6 - 2.6 mg/dl) with normal albumin, alkaline phosphatase and renal function test. She was diagnosed with pseudohypoparathyroidism and started on calcium and active vitamin D supplement and was referred for genetic testing study. She reported significant improvement in myalgia after a few weeks of starting calcium and active vitamin D supplementations and repeat lab testing showed improved hypocalcemia and hyperphosphatemia. This case illustrates unusual presentation of PTH resistance with basal ganglia calcification as initial presentation prompting further workup. She likely has pseudohypoparathyroidism type 1b. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism.
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Boughner, D. R., M. Thornton, J. Dunmore-Buyze, and D. W. Holdsworth. "The radiographic quantitation of aortic valve calcification: implications for assessing bioprosthetic valve calcificationin vitro." Physiological Measurement 21, no. 3 (August 1, 2000): 409–16. http://dx.doi.org/10.1088/0967-3334/21/3/306.
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Atkinson, Jeffrey. "Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences." Journal of Applied Physiology 105, no. 5 (November 2008): 1643–51. http://dx.doi.org/10.1152/japplphysiol.90476.2008.
Повний текст джерелаАнотація:
With age, the calcium content of the arterial wall increases. Calcification occurs at two main levels: intimal plaques and the medial elastic fiber network. The latter has been referred to as medial elastocalcinosis and is the subject of this review. The mechanisms involved in elastocalcinosis are complex and involve polar, apolar, and active processes. Vascular calcification may be species specific to humans. As laboratory animals, such as the rat, grow old, they suffer from only very mild arterial calcification. Different animal models of induction of massive arterial calcification by pharmacological and other means exist. Although extrapolation from such models to the clinical situation in terms of etiology is difficult, such models could be useful in the nonclinical study of the pathophysiological consequences of vascular calcification. Vascular calcification modifies arterial wall stiffness, and this could have clinically significant consequences on cardiac function and downstream circulatory control.
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Calabrò, Rocco Salvatore, Letteria Spadaro, Angela Marra, and Placido Bramanti. "Fahr’s Disease Presenting with Dementia at Onset: A Case Report and Literature Review." Behavioural Neurology 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/750975.
Повний текст джерелаАнотація:
Fahr’s disease (FD) is characterized by sporadic or familiar idiopathic calcification of the basal ganglia, dentate nuclei of the cerebellum, and centrum semiovale, mainly presenting with movement disorder, dementia, and behavioral abnormalities. We described a rare case of Fahr’s disease presenting at onset only with behavioral and neuropsychological alterations, whose diagnosis was supposed only after a brain CT, which showed extensive bilateral calcifications in the dentate nuclei of the cerebellum and basal ganglia. Since the onset of Fahr’s disease may be a dysexecutive syndrome with behavioral abnormalities, the clinical and radiological features are really important to do the appropriate diagnosis.
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Peralta-Ramírez, A., A. Montes de Oca, A. I. Raya, C. Pineda, I. López, F. Guerrero, E. Diez, et al. "Vitamin E protection of obesity-enhanced vascular calcification in uremic rats." American Journal of Physiology-Renal Physiology 306, no. 4 (February 15, 2014): F422—F429. http://dx.doi.org/10.1152/ajprenal.00355.2013.
Повний текст джерелаАнотація:
This study aimed to determine the extent of extraskeletal calcification in uremic Zucker rats, by comparing obese and lean phenotypes, and to evaluate the influence of vitamin E (VitE) on the development of calcifications in both uremic rats and human vascular smooth muscle cells (HVSMCs) cultured in vitro. Zucker rats of lean and obese phenotypes with normal renal function [control (C); C-lean and C-obese groups] and with uremia [5/6 nephrectomy (Nx); Nx-lean and Nx-obese groups] and uremic rats treated with VitE (Nx-lean + VitE and Nx-obese + VitE groups) were studied. Uremic groups were subjected to Nx, fed a 0.9% phosphorus diet, and treated with calcitriol (80 ng/kg ip). The aortic calcium concentration was significantly higher ( P < 0.05) in Nx-obese rats (10.0 ± 2.1 mg/g tissue) than in Nx-lean rats (3.6 ± 1.3 mg/g tissue). A decrease in plasma glutathione peroxidase activity was observed in Nx-obese rats compared with Nx-lean rats (217.2 ± 18.2 vs. 382.3 ± 15.5 nmol·min−1·ml−1, P < 0.05). Treatment with VitE restored glutathione peroxidase activity and reduced the aortic calcium concentration to 4.6 ± 1.3 mg/g tissue. The differences in mineral deposition between Nx-lean, Nx-obese, Nx-lean + VitE, and Nx-obese + VitE rats were also evidenced in other soft tissues. In HVSMCs incubated with high phosphate, VitE also prevented oxidative stress and reduced calcium content, bone alkaline phosphatase, and gene expression of core-binding factor-α1. In conclusion, uremic obese rats develop more severe calcifications than uremic lean rats and VitE reduces oxidative stress and vascular calcifications in both rats and cultures of HVSMCs.
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Gori, Andrea, Christine Ferrier-Pagès, Sebastian J. Hennige, Fiona Murray, Cécile Rottier, Laura C. Wicks, and J. Murray Roberts. "Physiological response of the cold-water coralDesmophyllum dianthusto thermal stress and ocean acidification." PeerJ 4 (February 2, 2016): e1606. http://dx.doi.org/10.7717/peerj.1606.
Повний текст джерелаАнотація:
Rising temperatures and ocean acidification driven by anthropogenic carbon emissions threaten both tropical and temperate corals. However, the synergistic effect of these stressors on coral physiology is still poorly understood, in particular for cold-water corals. This study assessed changes in key physiological parameters (calcification, respiration and ammonium excretion) of the widespread cold-water coralDesmophyllum dianthusmaintained for ∼8 months at two temperatures (ambient 12 °C and elevated 15 °C) and two pCO2conditions (ambient 390 ppm and elevated 750 ppm). At ambient temperatures no change in instantaneous calcification, respiration or ammonium excretion rates was observed at either pCO2levels. Conversely, elevated temperature (15 °C) significantly reduced calcification rates, and combined elevated temperature and pCO2significantly reduced respiration rates. Changes in the ratio of respired oxygen to excreted nitrogen (O:N), which provides information on the main sources of energy being metabolized, indicated a shift from mixed use of protein and carbohydrate/lipid as metabolic substrates under control conditions, to less efficient protein-dominated catabolism under both stressors. Overall, this study shows that the physiology ofD. dianthusis more sensitive to thermal than pCO2stress, and that the predicted combination of rising temperatures and ocean acidification in the coming decades may severely impact this cold-water coral species.
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Sakai, H., and N. Nakamura. "Physiological calcification of the septum pellucidum." Neuroradiology 28, no. 2 (March 1986): 173. http://dx.doi.org/10.1007/bf00327893.
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Korff, Susanne, Frank Schoensiegel, Nora Riechert, Dieter Weichenhan, Hugo A. Katus, and Boris T. Ivandic. "Fine mapping of Dyscalc1, the major genetic determinant of dystrophic cardiac calcification in mice." Physiological Genomics 25, no. 3 (May 16, 2006): 387–92. http://dx.doi.org/10.1152/physiolgenomics.00010.2006.
Повний текст джерелаАнотація:
Calcification of severely dystrophic muscle is occasionally observed in targeted mouse models of muscular dystrophy and cardiomyopathy. Intracellular calcium deposition occurs in necrotic myocytes in the absence of plasma calcium and phosphate imbalances. In the heart, this recessive trait is referred to as dystrophic cardiac calcinosis (DCC). We identified previously Dyscalc1, a major genetic determinant of DCC, in a 15.2-Mbp region on proximal chromosome 7. We report now further steps toward the identification of the Dyscalc1 gene by reverse genetics. Transferring the Dyscalc1 locus from susceptible mouse strain C3H/He onto a resistant C57BL/6 strain background, we generated congenic inbred strains B6.C3-( D7Mit56-D7Mit230) and B6.C3-( D7Nds5-D7Mit230). Three days after myocardial freeze-thaw injury, both strains exhibited calcification of necrotic lesions, confirming the pathogenetic relevance of Dyscalc1. Analysis of two (129S1 × C57BL/6) × 129S1 backcrosses allowed mapping of Dyscalc1 more precisely to a region spanning 0.76 Mbp between genes Fgf21 (39.70 Mbp) and Myod1 (40.46 Mbp). This interval contains 31 known and putative genes in three large, ancestral haplotypes shared by susceptible strains C3H/He, 129S1, and DBA/2. Thus we were able to exclude previously proposed candidate genes Bax and Hrc. Instead, a potential candidate may be the gene encoding the ATP-binding cassette C6. Mutations in the orthologous human ABCC6 gene cause pseudoxanthoma elasticum, or Gronblad-Strandberg syndrome, an elastic tissue disorder with cardiovascular calcifications.
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Chapperon, Coraline, Jacques Clavier, Clément Dugué, Erwan Amice, Manon Le Goff, and Sabine Roussel. "Seasonal and diurnal variability in carbon respiration, calcification and excretion rates of the abalone Haliotis tuberculata L." Journal of the Marine Biological Association of the United Kingdom 99, no. 2 (March 12, 2018): 393–402. http://dx.doi.org/10.1017/s0025315418000097.
Повний текст джерелаАнотація:
Abalone (Haliotis spp.) are commercially important marine shellfish species worldwide. Knowledge about the physiology of abalone that impacts life-history traits is important for a better understanding of the biology of the species and the impact of stressful husbandry procedures at different seasons. The present study quantified the seasonal and diurnal variations in four physiological parameters of the European species Haliotis tuberculata, i.e. carbon aerial and aquatic respiration, calcification and excretion rates, and the effect of prolonged aerial exposure upon abalone aerial respiration. We also investigated the effect of individual size upon these physiological parameters. Aquatic respiration and calcification rates showed an allometric relationship with biomass. All parameters showed lower rates in cool season and higher rates in warmer season. Temperature was assumed to be the primary driver of the reported seasonal variability in physiological parameters, although reproductive needs and nutrition may also contribute to the observed patterns. Importantly, abalone did not stop calcifying in winter, and calcified more at night than during the day. Abalone did not respire more underwater at night-time than at daytime, however they excreted more overnight. The low air:aquatic ratio (0.2) is likely to be an energy-saving strategy for emerged H. tuberculata individuals. This study highlights the temporal heterogeneity in physiological rates of H. tuberculata, which constitutes a species recently domesticated in Europe.
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Opdebeeck, Britt, Isabel R. Orriss, Ellen Neven, Patrick C. D’Haese, and Anja Verhulst. "Extracellular Nucleotides Regulate Arterial Calcification by Activating Both Independent and Dependent Purinergic Receptor Signaling Pathways." International Journal of Molecular Sciences 21, no. 20 (October 15, 2020): 7636. http://dx.doi.org/10.3390/ijms21207636.
Повний текст джерелаАнотація:
Arterial calcification, the deposition of calcium-phosphate crystals in the extracellular matrix, resembles physiological bone mineralization. It is well-known that extracellular nucleotides regulate bone homeostasis raising an emerging interest in the role of these molecules on arterial calcification. The purinergic independent pathway involves the enzymes ecto-nucleotide pyrophosphatase/phosphodiesterases (NPPs), ecto-nucleoside triphosphate diphosphohydrolases (NTPDases), 5′-nucleotidase and alkaline phosphatase. These regulate the production and breakdown of the calcification inhibitor—pyrophosphate and the calcification stimulator—inorganic phosphate, from extracellular nucleotides. Maintaining ecto-nucleotidase activities in a well-defined range is indispensable as enzymatic hyper- and hypo-expression has been linked to arterial calcification. The purinergic signaling dependent pathway focusses on the activation of purinergic receptors (P1, P2X and P2Y) by extracellular nucleotides. These receptors influence arterial calcification by interfering with the key molecular mechanisms underlying this pathology, including the osteogenic switch and apoptosis of vascular cells and possibly, by favoring the phenotypic switch of vascular cells towards an adipogenic phenotype, a recent, novel hypothesis explaining the systemic prevention of arterial calcification. Selective compounds influencing the activity of ecto-nucleotidases and purinergic receptors, have recently been developed to treat arterial calcification. However, adverse side-effects on bone mineralization are possible as these compounds reasonably could interfere with physiological bone mineralization.
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Findlay, H. S., H. L. Wood, M. A. Kendall, J. I. Spicer, R. J. Twitchett, and S. Widdicombe. "Calcification, a physiological process to be considered in the context of the whole organism." Biogeosciences Discussions 6, no. 1 (February 24, 2009): 2267–84. http://dx.doi.org/10.5194/bgd-6-2267-2009.
Повний текст джерелаАнотація:
Abstract. Marine organisms that produce calcium carbonate structures are predicted to be most vulnerable to a decline in oceanic pH (ocean acidification) based on the understanding that calcification rates will decrease as a result of changes in the seawater carbonate chemistry thereby reducing carbonate ion concentration (and associated saturation states). Coastal seas are critical components of the global carbon cycle yet little research has been conducted on acidification impacts on coastal benthic organisms. Here, a critical appraisal of calcification in six benthic species showed, contrary to popular predictions, calcification can increase, and not decrease, in acidified seawater. Measuring the changes in calcium in isolated calcium carbonate structure as well as structures from live animals exposed to acidified seawater allowed a comparison between a species' ability to calcify and the dissolution affects across decreasing levels of pH. Calcium carbonate production is dependant on the ability to increase calcification thus counteracting an increase in dissolution. Comparison with paleoecological studies of past high carbon dioxide (CO2) events presents a similar picture. This conclusion implies that calcification may not be the critical process impacted by ocean acidification; particularly as all species investigated displayed physiological trade offs including reduced metabolism, health, and behavioural responses, in association with this calcification upregulation, which possess as great a threat to survival as an inability to calcify.
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Lohbeck, Kai T., Ulf Riebesell, and Thorsten B. H. Reusch. "Gene expression changes in the coccolithophore Emiliania huxleyi after 500 generations of selection to ocean acidification." Proceedings of the Royal Society B: Biological Sciences 281, no. 1786 (July 7, 2014): 20140003. http://dx.doi.org/10.1098/rspb.2014.0003.
Повний текст джерелаАнотація:
Coccolithophores are unicellular marine algae that produce biogenic calcite scales and substantially contribute to marine primary production and carbon export to the deep ocean. Ongoing ocean acidification particularly impairs calcifying organisms, mostly resulting in decreased growth and calcification. Recent studies revealed that the immediate physiological response in the coccolithophore Emiliania huxleyi to ocean acidification may be partially compensated by evolutionary adaptation, yet the underlying molecular mechanisms are currently unknown. Here, we report on the expression levels of 10 candidate genes putatively relevant to pH regulation, carbon transport, calcification and photosynthesis in E. huxleyi populations short-term exposed to ocean acidification conditions after acclimation (physiological response) and after 500 generations of high CO 2 adaptation (adaptive response). The physiological response revealed downregulation of candidate genes, well reflecting the concomitant decrease of growth and calcification. In the adaptive response, putative pH regulation and carbon transport genes were up-regulated, matching partial restoration of growth and calcification in high CO 2 -adapted populations. Adaptation to ocean acidification in E. huxleyi likely involved improved cellular pH regulation, presumably indirectly affecting calcification. Adaptive evolution may thus have the potential to partially restore cellular pH regulatory capacity and thereby mitigate adverse effects of ocean acidification.
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Wall, C. B., R. A. B. Mason, W. R. Ellis, R. Cunning, and R. D. Gates. "Elevated p CO 2 affects tissue biomass composition, but not calcification, in a reef coral under two light regimes." Royal Society Open Science 4, no. 11 (November 2017): 170683. http://dx.doi.org/10.1098/rsos.170683.
Повний текст джерелаАнотація:
Ocean acidification (OA) is predicted to reduce reef coral calcification rates and threaten the long-term growth of coral reefs under climate change. Reduced coral growth at elevated p CO 2 may be buffered by sufficiently high irradiances; however, the interactive effects of OA and irradiance on other fundamental aspects of coral physiology, such as the composition and energetics of coral biomass, remain largely unexplored. This study tested the effects of two light treatments (7.5 versus 15.7 mol photons m −2 d −1 ) at ambient or elevated p CO 2 (435 versus 957 µatm) on calcification, photopigment and symbiont densities, biomass reserves (lipids, carbohydrates, proteins), and biomass energy content (kJ) of the reef coral Pocillopora acuta from Kāne‘ohe Bay, Hawai‘i. While p CO 2 and light had no effect on either area- or biomass-normalized calcification, tissue lipids gdw −1 and kJ gdw −1 were reduced 15% and 14% at high p CO 2 , and carbohydrate content increased 15% under high light. The combination of high light and high p CO 2 reduced protein biomass (per unit area) by approximately 20%. Thus, under ecologically relevant irradiances, P. acuta in Kāne‘ohe Bay does not exhibit OA-driven reductions in calcification reported for other corals; however, reductions in tissue lipids, energy content and protein biomass suggest OA induced an energetic deficit and compensatory catabolism of tissue biomass. The null effects of OA on calcification at two irradiances support a growing body of work concluding some reef corals may be able to employ compensatory physiological mechanisms that maintain present-day levels of calcification under OA. However, negative effects of OA on P. acuta biomass composition and energy content may impact the long-term performance and scope for growth of this species in a high p CO 2 world.
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Thomsen, J., K. Haynert, K. M. Wegner, and F. Melzner. "Impact of seawater carbonate chemistry on the calcification of marine bivalves." Biogeosciences 12, no. 14 (July 17, 2015): 4209–20. http://dx.doi.org/10.5194/bg-12-4209-2015.
Повний текст джерелаАнотація:
Abstract. Bivalve calcification, particularly of the early larval stages, is highly sensitive to the change in ocean carbonate chemistry resulting from atmospheric CO2 uptake. Earlier studies suggested that declining seawater [CO32−] and thereby lowered carbonate saturation affect shell production. However, disturbances of physiological processes such as acid-base regulation by adverse seawater pCO2 and pH can affect calcification in a secondary fashion. In order to determine the exact carbonate system component by which growth and calcification are affected it is necessary to utilize more complex carbonate chemistry manipulations. As single factors, pCO2 had no effects and [HCO3-] and pH had only limited effects on shell growth, while lowered [CO32−] strongly impacted calcification. Dissolved inorganic carbon (CT) limiting conditions led to strong reductions in calcification, despite high [CO32−], indicating that [HCO3-] rather than [CO32−] is the inorganic carbon source utilized for calcification by mytilid mussels. However, as the ratio [HCO3-] / [H+] is linearly correlated with [CO32−] it is not possible to differentiate between these under natural seawater conditions. An equivalent of about 80 μmol kg−1 [CO32−] is required to saturate inorganic carbon supply for calcification in bivalves. Below this threshold biomineralization rates rapidly decline. A comparison of literature data available for larvae and juvenile mussels and oysters originating from habitats differing substantially with respect to prevailing carbonate chemistry conditions revealed similar response curves. This suggests that the mechanisms which determine sensitivity of calcification in this group are highly conserved. The higher sensitivity of larval calcification seems to primarily result from the much higher relative calcification rates in early life stages. In order to reveal and understand the mechanisms that limit or facilitate adaptation to future ocean acidification, it is necessary to better understand the physiological processes and their underlying genetics that govern inorganic carbon assimilation for calcification.
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de Nooijer, L. J., G. Langer, G. Nehrke, and J. Bijma. "Physiological controls on seawater uptake and calcification in the benthic foraminifer <i>Ammonia tepida</i>." Biogeosciences Discussions 6, no. 4 (July 16, 2009): 7083–102. http://dx.doi.org/10.5194/bgd-6-7083-2009.
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Abstract. During the last decades conceptual models describing the calcification pathway of foraminifera and its physiological controls have been developed. These models are derived by combining data of tracer experiments and microscopic observations obtained from different species. Although vital for understanding their calcitic isotopic and trace elemental composition, direct observational evidence on e.g. seawater vacuolization and intracellular Ca-cycling is lacking for most species. To analyse the relation between seawater uptake and calcification, we incubated juveniles of the cosmopolitan benthic, intertidal foraminifer Ammonia tepida with various fluorescent probes. Visualizing the membranes of endocytosed vesicles was achieved by incubating specimens with the dye FM1-43, while Ca ions in the calcification vesicles were detected by the Ca2+-indicator Fluo3-AM. Uptake of fluorescent latex-beads (0.5 μm diameter) and subsequent transport to the site of chamber formation provided additional evidence that endocytosis is related to the calcification pathway and not merely involved in membrane cycling. Our results show for the first time that endocytosis of seawater is part of the calcification process in Ammonia tepida. Data on the intracellular calcium ion-cycling allowed for calculating a preliminary cellular Ca-budget during foraminiferal calcification.
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Chen, Qiang, Ze-Yang Wang, Li-Yuan Chen, and Hou-Yuan Hu. "Roles of High Mobility Group Box 1 in Cardiovascular Calcification." Cellular Physiology and Biochemistry 42, no. 2 (2017): 427–40. http://dx.doi.org/10.1159/000477591.
Повний текст джерелаАнотація:
Calcific disease of the cardiovascular system, including atherosclerotic calcification, medial calcification in diabetes and calcific aortic valve disease, is an important risk factor for many adverse cardiovascular events such as ischemic cardiac events and subsequent mortality. Although cardiovascular calcification has long been considered to be a passive degenerative occurrence, it is now recognized as an active and highly regulated process that involves osteochondrogenic differentiation, apoptosis and extracellular vesicle release. Nonetheless, despite numerous studies on the pathogenesis of cardiovascular calcification, the underlying mechanisms remain poorly understood. High mobility group box 1 (HMGB1), a nuclear protein bound to chromatin in almost all eukaryotic cells, acts as a damage-associated molecular pattern (DAMP) when released into the extracellular space upon cell activation, injury or death. Moreover, HMGB1 also functions as a bone-active cytokine participating in bone remodeling and ectopic calcification pathogenesis. However, studies on the roles of HMGB1 in promoting cardiovascular calcification are limited to date, and the mechanisms involved are still unclear. In this review, we summarize recent studies investigating the mechanism of cardiovascular calcification and discuss multiple roles of HMGB1 in its development.
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Thomsen, J., K. Haynert, K. M. Wegner, and F. Melzner. "Impact of seawater carbonate chemistry on the calcification of marine bivalves." Biogeosciences Discussions 12, no. 2 (January 22, 2015): 1543–71. http://dx.doi.org/10.5194/bgd-12-1543-2015.
Повний текст джерелаАнотація:
Abstract. Bivalve calcification, particular of the early larval stages is highly sensitive to the change of ocean carbonate chemistry resulting from atmospheric CO2 uptake. Earlier studies suggested that declining seawater [CO32−] and thereby lowered carbonate saturation affect shell production. However, disturbances of physiological processes such as acid-base regulation by adverse seawater pCO2 and pH can affect calcification in a secondary fashion. In order to determine the exact carbonate system component by which growth and calcification are affected it is necessary to utilize more complex carbonate chemistry manipulations. As single factors, pCO2 had no and [HCO3−] and pH only limited effects on shell growth, while lowered [CO32−] strongly impacted calcification. Dissolved inorganic carbon (CT) limiting conditions led to strong reductions in calcification, despite high [CO32−], indicating that [HCO3−] rather than [CO32−] is the inorganic carbon source utilized for calcification by mytilid mussels. However, as the ratio [HCO3−] / [H&plus;] is linearly correlated with [CO32−] it is not possible to differentiate between these under natural seawater conditions. Therefore, the availability of [HCO3−] combined with favorable environmental pH determines calcification rate and an equivalent of about 80 μmol kg−1 [CO32−] is required to saturate inorganic carbon supply for calcification in bivalves. Below this threshold biomineralization rates rapidly decline. A comparison of literature data available for larvae and juvenile mussels and oysters originating from habitats differing substantially with respect to prevailing carbonate chemistry conditions revealed similar response curves. This suggests that the mechanisms which determine sensitivity of calcification in this group are highly conserved. The higher sensitivity of larval calcification seems to primarily result from the much higher relative calcification rates in early life stages. In order to reveal and understand the mechanisms that limit or facilitate adaptation to future ocean acidification, it is necessary to better understand the physiological processes and their underlying genetics that govern inorganic carbon assimilation for calcification.
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Meng, Fanxing, Yonggang Zhao, Bing Wang, Bingwei Li, Youming Sheng, Mingming Liu, Hongwei Li, and Ruijuan Xiu. "Endothelial Cells Promote Calcification in Aortic Smooth Muscle Cells from Spontaneously Hypertensive Rats." Cellular Physiology and Biochemistry 49, no. 6 (2018): 2371–81. http://dx.doi.org/10.1159/000493837.
Повний текст джерелаАнотація:
Background/Aims: Vascular calcification and hypertension are intimately linked, and the progression of hypertension is closely correlated with endothelial dysfunction. However, the role of endothelial cells (ECs) in vascular calcification of hypertension remains unclear. Therefore, the present study explored the effects of ECs on calcification of smooth muscle cells (SMCs) from aortas of spontaneously hypertensive rats (SHR). Methods: Aortic ECs and SMCs were isolated from SHR and Wistar rats, respectively. The roles of ECs in the regulation of SMCs calcification were investigated by co-culture and conditioned culture model. Calcium deposition of SMCs was detected by von Kossa staining. Quantization of calcium content in SMCs was determined colorimetrically by the o-cresolphthalein complexone method. Alkaline phosphatase (ALP) activity was measured colorimetrically by p-nitrophenol. The expression levels of MMP-2, MMP-9 and the calcification-promoting proteins were analyzed by Western blot. Results: Calcium deposition, ALP activity and the expression levels of calcification-promoting proteins in SMCs of SHR were significantly higher than that cultured without ECs after 6 days of co-culture with ECs or conditioned culture with the medium of ECs, however, there were no statistical differences between SMCs of Wistar rats. MMP-2 and MMP-9 in co-cultured ECs from SHR were dramatically higher than that cultured without SMCs, nevertheless, there were no statistical differences between ECs from Wistar rats and between SMCs from SHR or Wistar rats. Moreover, SB-3CT, a specific inhibitor of gelatinases, decreased calcium content and the expression levels of calcification-promoting proteins in both co-cultured and conditionally cultured SMCs from SHR. Conclusion: ECs have the ability to promote calcification of aortic SMCs of SHR, and elevated expressions of MMP-2 and MMP-9 in ECs of SHR might facilitate the calcification of SMCs.
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Carracedo, Miguel, Gonzalo Artiach, Anna Witasp, Joan Clària, Mattias Carlström, Andres Laguna-Fernandez, Peter Stenvinkel, and Magnus Bäck. "The G-protein coupled receptor ChemR23 determines smooth muscle cell phenotypic switching to enhance high phosphate-induced vascular calcification." Cardiovascular Research 115, no. 10 (December 28, 2018): 1557–66. http://dx.doi.org/10.1093/cvr/cvy316.
Повний текст джерелаАнотація:
Abstract Aims Vascular calcification, a marker of increased cardiovascular risk, is an active process orchestrated by smooth muscle cells. Observational studies indicate that omega-3 fatty acids protect against vascular calcification, but the mechanisms are unknown. The G-protein coupled receptor ChemR23 transduces the resolution of inflammation induced by the omega-3-derived lipid mediator resolvin E1. ChemR23 also contributes to osteoblastic differentiation of stem cells and bone formation, but its role in vascular calcification is unknown. The aim of this study was to establish the role of ChemR23 in smooth muscle cell fate and calcification Methods and results Gene expression analysis in epigastric arteries derived from patients with chronic kidney disease and vascular calcification revealed that ChemR23 mRNA levels predicted a synthetic smooth muscle cell phenotype. Genetic deletion of ChemR23 in mice prevented smooth muscle cell de-differentiation. ChemR23-deficient smooth muscle cells maintained a non-synthetic phenotype and exhibited resistance to phosphate-induced calcification. Moreover, ChemR23-deficient mice were protected against vitamin D3-induced vascular calcification. Resolvin E1 inhibited smooth muscle cell calcification through ChemR23. Introduction of the Caenorhabditis elegans Fat1 transgene, leading to an endogenous omega-3 fatty acid synthesis and hence increased substrate for resolvin E1 formation, significantly diminished the differences in phosphate-induced calcification between ChemR23+/+ and ChemR23−/− mice. Conclusion This study identifies ChemR23 as a previously unrecognized determinant of synthetic and osteoblastic smooth muscle cell phenotype, favouring phosphate-induced vascular calcification. This effect may be of particular importance in the absence of ChemR23 ligands, such as resolvin E1, which acts as a calcification inhibitor under hyperphosphatic conditions.
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Bayrak, Seval, Duygu Göller Bulut, Emine Şebnem Kurşun Çakmak, and Kaan Orhan. "Cone Beam Computed Tomographic Evaluation of Intracranial Physiologic Calcifications." Journal of Craniofacial Surgery 30, no. 2 (2019): 510–13. http://dx.doi.org/10.1097/scs.0000000000004918.
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Lee, Chi H. "Physiological variables involved in heart valve substitute calcification." Expert Opinion on Biological Therapy 9, no. 8 (June 26, 2009): 1031–42. http://dx.doi.org/10.1517/14712590903085091.
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Shuvy, Mony, Suzan Abedat, Ronen Beeri, Michael Valitsky, Sameh Daher, Miriam Kott-Gutkowski, Anca Gal-Moscovici, Jacob Sosna, Nalini M. Rajamannan, and Chaim Lotan. "Raloxifene attenuates Gas6 and apoptosis in experimental aortic valve disease in renal failure." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1829—H1840. http://dx.doi.org/10.1152/ajpheart.00240.2010.
Повний текст джерелаАнотація:
Renal failure is associated with aortic valve calcification. Using our rat model of uremia-induced reversible aortic valve calcification, we assessed the role of apoptosis and survival pathways in that disease. We also explored the effects of raloxifene, an estrogen receptor modulator, on valvular calcification. Gene array analysis was performed in aortic valves obtained from three groups of rats ( n = 7 rats/group): calcified valves obtained from rats fed with uremic diet, valves after calcification resolution following diet cessation, and control. In addition, four groups of rats ( n = 10 rats/group) were used to evaluate the effect of raloxifene in aortic valve calcification: three groups as mentioned above and a fourth group fed with the uremic diet that also received daily raloxifene. Evaluation included imaging, histology, and antigen expression analysis. Gene array results showed that the majority of the altered expressed genes were in diet group valves. Most apoptosis-related genes were changed in a proapoptotic direction in calcified valves. Apoptosis and decreases in several survival pathways were confirmed in calcified valves. Resolution of aortic valve calcification was accompanied by decreased apoptosis and upregulation of survival pathways. Imaging and histology demonstrated that raloxifene significantly decreased aortic valve calcification. In conclusion, downregulation of several survival pathways and apoptosis are involved in the pathogenesis of aortic valve calcification. The beneficial effect of raloxifene in valve calcification is related to apoptosis modulation. This novel observation is important for developing remedies for aortic valve calcification in patients with renal failure.
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Bobryshev, Yuri V., Reginald S. A. Lord, and Dinh Tran. "Chlamydia pneumoniaein foci of “early” calcification of the tunica media in arteriosclerotic arteries: an incidental presence?" American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (April 2006): H1510—H1519. http://dx.doi.org/10.1152/ajpheart.01055.2005.
Повний текст джерелаАнотація:
Only a few previous works investigated the involvement of Chlamydia pneumoniae ( Chlamydophila pneumoniae) in arterial calcification. The present study investigated a possible association between C. pneumoniae and medial calcification. Carotid artery segments obtained by endarterectomy from 60 patients were examined by PCR and immunohistochemistry to identify the presence of C. pneumoniae. Arterial specimens showing double-positive ( n = 17), double-negative ( n = 22), and single-positive results ( n = 21) were further analyzed by a combination of histology, immunohistochemistry, and electron microscopy. Medial calcification occurred in 10 of 17 (58.8%) C. pneumoniae double-positive arterial specimens, but no medial calcification was observed in any of 22 C. pneumoniae double-negative arterial specimens. Electron microscopy indicated C. pneumoniae in smooth muscle cells (SMCs) in foci of medial calcification. Medial SMCs showing damage to the cytoplasm and basement membrane contained the structures with the appearance of elementary, reticulate, and aberrant bodies of C. pneumoniae. The presence of C. pneumoniae in SMCs was confirmed by electron-microscopic immunocytochemistry. In the extracellular matrix, calcification was observed in C. pneumoniae aberrant bodies that exited the SMCs. The findings offer a new hypothesis of arterial calcification: they suggest that C. pneumoniae infection of medial SMCs may be associated with the pathophysiological events of arteriosclerotic calcification of the tunica media.