• Title/Summary/Keyword: calcification

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Frequency, shape, and estimated volume of intracranial physiologic calcification in different age groups investigated by brain computed tomography scan: a retrospective study

  • Mehrdad Ghorbanlou;Fatemeh Moradi;Mehdi Mehdizadeh
    • Anatomy and Cell Biology
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    • v.55 no.1
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    • pp.63-71
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    • 2022
  • Intracranial calcification is referred to calcification of parenchyma and vascular structures in brain which can be physiologic or pathologic. This study was conducted with the purpose of investigating the frequency, location, pattern, dimensions and estimated volume of intracranial physiologic calcification (IPC) by computer tomography in different age groups. In this cross-sectional retrospective study, brain computed tomography scans of 216 patients were analyzed in 9 age groups each containing 24 patients from 2 to 89 years old. Data were analyzed by SPSS software using one way analysis of variance (ANOVA, post hoc Tukey), chi square, and linear regression tests (P≤0.05 was considered significant). Rate of calcification in different areas were as follows: pineal gland (75.0%), habenula (36.4%), pineohabenula (15.0%), right lateral ventricle choroid plexus (RCP) (67.7%), left lateral ventricle choroid plexus (LCP) (62.7%), falx cerebri (26.8%), petroclinoid ligament (13.2%), tentorium cerebelli (6.8%), third ventricle choroid plexus (0.9%), fourth ventricle choroid plexus (2.7%), basal ganglia (0.9%). A significant correlation exists between the presence of calcification in pineal, habenula, RCP, and LCP (P≤0.001). Nodular shape of calcification was dominant (47.9%). Estimated volume of pineal calcification showed increased levels in group 8 (70-79 years old) compared to group 2 (10-19 years old) (P≤0.05). Since the accurate description of radiologic appearance of IPCs (location, shape, and size) accompanied with age and clinical manifestation is of great importance in diagnosis and distinguishing from pathologic calcification-for example in patients with melatonin dysregulation or schizophrenic patients-this study was required.

Intracranial Calcification Caused by a Brain Abscess : A Rare Cause of Intracranial Calcification

  • Kim, Hyeun Sook;Kim, Dong Min;Ju, Chang Il;Kim, Seok Won
    • Journal of Korean Neurosurgical Society
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    • v.54 no.2
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    • pp.148-150
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    • 2013
  • Intracranial calcifications are relatively common computed tomographic findings in the field of neurosurgery, and cysticercosis, tuberculosis, HIV, and cryptococcus are acquired intracranial infections typically associated with calcifications. However, intracranial calcification caused by a bacterial brain abscess is rare. Here, we present a rare case of intracranial calcification caused by a bacterial brain abscess, from which staphylococcus hominis was isolated. To the best of our knowledge, no previous report has been published on intracranial calcification caused by bacterial brain abscess after decompressive craniectomy for traumatic brain injury. In this article, the pathophysiological mechanism of this uncommon entity is discussed and relevant literature reviewed.

Neuromedin B modulates phosphate-induced vascular calcification

  • Park, Hyun-Joo;Kim, Mi-Kyoung;Kim, Yeon;Kim, Hyung Joon;Bae, Soo-Kyung;Bae, Moon-Kyoung
    • BMB Reports
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    • v.54 no.11
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    • pp.569-574
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    • 2021
  • Vascular calcification is the heterotopic accumulation of calcium phosphate salts in the vascular tissue and is highly correlated with increased cardiovascular morbidity and mortality. In this study, we found that the expression of neuromedin B (NMB) and NMB receptor is upregulated in phosphate-induced calcification of vascular smooth muscle cells (VSMCs). Silencing of NMB or treatment with NMB receptor antagonist, PD168368, inhibited the phosphate-induced osteogenic differentiation of VSMCs by inhibiting Wnt/β-catenin signaling and VSMC apoptosis. PD168368 also attenuated the arterial calcification in cultured aortic rings and in a rat model of chronic kidney disease. The results of this study suggest that NMB-NMB receptor axis may have potential therapeutic value in the diagnosis and treatment of vascular calcification.

The relation of the bioprosthetic valve failure to its calcification (조직판막의 실패와 석회화에 관한 연구)

  • 홍유선
    • Journal of Chest Surgery
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    • v.22 no.6
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    • pp.1001-1012
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    • 1989
  • In 1968, Carpentier and his associates introduced glutaraldehyde as a compound for preparing cardiac tissue valve, and this technique has provided a considerably more suitable and durable tissue valve substitute. To increase further durability of valve tissue, Reis and his colleagues designed a flexible stent to reduce the stress on the heterogeneous tissue valve mounted. However with the advent of more innovative mechanical valve currently, many bioprosthetic valves are being substituted by mechanical valves at our department of cardiothoracic surgery because of bioprosthetic valve failure. Main cause of bioprosthetic valves failure were calcification or/and tear of tissue valves. The purpose of this retrospective study is to clarify the relationship between the patients clinical profile during implantation of tissue valves and pathologic features of the failed bioprosthetic valve. From March, 1982 through June, 1988, 53 bioprosthetic heart valves that had been ex-planted from 45 patients at the department of cardiac surgery of Yonsei University Hospital were subjected to this study. The patients were 10 to 65 year-old [mean age: 30.3 yr] with 17 males and 28 females. Re-replacements of prosthetic valves were carried out twenty nine in mitral position, eight in aortic position and eight in both aortic and mitral position simultaneously. The grading and location for calcification of valves were verified by radiograms. The calcification of the explanted valves leaflets was graded from 0 to 4 plus according to Cipriano and associates method. The types of tear and perforation of leaflet were classified into four types as Ishihara has adopted initially in 1981. In younger age group under thirty three years, explanted tissue valves were significantly more affected in terms of grades of severity of valve calcification as compared with older age group [p < 0.035]. Valve calcification appeared more severe in male as compared to female [p< 0.002]. Ionescu-Shiley bovine pericardial bioprosthetic valves showed more severe calcification than Hancock porcine tissue valves [p< 0.035]. Calcium deposit was found very prevalent at the area of commissural attachment [86 % of all]. Type I of valve rupture was shown to be related with simultaneous calcification. However, the relation of explanted valve position, duration of implanted prosthetic valve, atrial fibrillation and anticoagulant therapy to the severity of bioprosthetic valve calcification were not significantly clear statistically [p > 0.05].

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Niclosamide Inhibits Aortic Valve Interstitial Cell Calcification by Interfering with the GSK-3β/β-Catenin Signaling Pathway

  • Radhika Adhikari;Saugat Shiwakoti;Eunmin Kim;Ik Jun Choi;Sin-Hee Park;Ju-Young Ko;Kiyuk Chang;Min-Ho Oak
    • Biomolecules & Therapeutics
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    • v.31 no.5
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    • pp.515-525
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    • 2023
  • The most common heart valve disorder is calcific aortic valve stenosis (CAVS), which is characterized by a narrowing of the aortic valve. Treatment with the drug molecule, in addition to surgical and transcatheter valve replacement, is the primary focus of researchers in this field. The purpose of this study is to determine whether niclosamide can reduce calcification in aortic valve interstitial cells (VICs). To induce calcification, cells were treated with a pro-calcifying medium (PCM). Different concentrations of niclosamide were added to the PCM-treated cells, and the level of calcification, mRNA, and protein expression of calcification markers was measured. Niclosamide inhibited aortic valve calcification as observed from reduced alizarin red s staining in niclosamide treated VICs and also decreased the mRNA and protein expressions of calcification-specific markers: runt-related transcription factor 2 and osteopontin. Niclosamide also reduced the formation of reactive oxygen species, NADPH oxidase activity and the expression of Nox2 and p22phox. Furthermore, in calcified VICs, niclosamide inhibited the expression of β-catenin and phosphorylated glycogen synthase kinase (GSK-3β), as well as the phosphorylation of AKT and ERK. Taken together, our findings suggest that niclosamide may alleviate PCM-induced calcification, at least in part, by targeting oxidative stress mediated GSK-3β/β-catenin signaling pathway via inhibiting activation of AKT and ERK, and may be a potential treatment for CAVS.

Malignancy Risk Stratification of Thyroid Nodules with Macrocalcification and Rim Calcification Based on Ultrasound Patterns

  • Hwa Seon Shin;Dong Gyu Na;Wooyul Paik;So Jin Yoon;Hye Yun Gwon;Byeong-Joo Noh;Won Jun Kim
    • Korean Journal of Radiology
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    • v.22 no.4
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    • pp.663-671
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    • 2021
  • Objective: To determine the association of macrocalcification and rim calcification with malignancy and to stratify the malignancy risk of thyroid nodules with macrocalcification and rim calcification based on ultrasound (US) patterns. Materials and Methods: The study included a total of 3603 consecutive nodules (≥ 1 cm) with final diagnoses. The associations of macrocalcification and rim calcification with malignancy and malignancy risk of the nodules were assessed overall and in subgroups based on the US patterns of the nodules. The malignancy risk of the thyroid nodules was categorized as high (> 50%), intermediate (upper-intermediate: > 30%, ≤ 50%; lower-intermediate: > 10%, ≤ 30%), and low (≤ 10%). Results: Macrocalcification was independently associated with malignancy in all nodules and solid hypoechoic (SH) nodules (p < 0.001). Rim calcification was not associated with malignancy in all nodules (p = 0.802); however, it was independently associated with malignancy in partially cystic or isoechoic and hyperechoic (PCIH) nodules (p = 0.010). The malignancy risks of nodules with macrocalcification were classified as upper-intermediate and high in SH nodules, and as low and lower-intermediate in PCIH nodules based on suspicious US features. The malignancy risks of nodules with rim calcification were stratified as low and lower-intermediate based on suspicious US features. Conclusion: Macrocalcification increased the malignancy risk in all and SH nodules with or without suspicious US features, with low to high malignancy risks depending on the US patterns. Rim calcification increased the malignancy risk in PCIH nodules, with low and lower-intermediate malignancy risks based on suspicious US features. However, the role of rim calcification in risk stratification of thyroid nodules remains uncertain.

Effect of Phosphate Binders on Vascular Calcification and Mortality in Korean Patients with Chronic Kidney Disease (만성신부전 환자의 혈관 석회화와 사망률에 미치는 인결합제의 영향)

  • Sin, Hye Yeon
    • Korean Journal of Clinical Pharmacy
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    • v.24 no.3
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    • pp.199-205
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    • 2014
  • Objectives: Current studies are debating on the association of vascular calcification and the benefit of treatment to lower serum phosphorus level in patients with chronic kidney disease. The aim of this study was to evaluate the association of mortality and risk of vascular calcification in patients with CKD who were taking phosphate binders. Methods: This study was conducted through retrospective medical chart review for 420 patients aged 18 years and older who were admitted for chronic kidney disease. Results: Vascular calcification was not statistically significantly associated with increased mortality in patients with CKD [16.7% vs. 19.2%; 95% CI; 0.388 to 1.818 (p=0.656)]. Intervention of calcium-based phosphate binders was not significantly associated with vascular calcification in patients with CKD [9.1% vs. 12.5%; 95% CI; 0.364 to 1.358 (p=0.292)]. Ca x P product ${\geq}55mg^2/dL^2$ was not significantly associated with increased 1 year mortality in patients with CKD [25.4% vs. 17.5%; 95% CI; 0.851 to 3.013 (p=0.142)]. Intervention of sevelamer was significantly associated with reduced 1 year mortality in patients with CKD than that of patients who did not take sevelamer [6.3% vs. 25.3%; 95% CI; 0.044 to 0.880 (p=0.020)]. Conclusion: There was not a statistically significant association between vascular calcification and phosphate binder's use. But phosphate binder use was significantly associated with decreased mortality in patients with CKD.

Inhibitory Effect of Fermented Spanish Extract on Inorganic phosphate-induced Vascular Calcification in ex vivo Aortic Rings (발효 시금치 추출물의 무기인산염에 의해 유도된 혈관 석회화 저해 효과)

  • Lee, Sang Hee;Hong, Sun Mi;Sung, Mi Jeong
    • Journal of the Korean Society of Food Culture
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    • v.37 no.3
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    • pp.248-255
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    • 2022
  • Spinach (Spinacia oleracea L.), a green leafy vegetable, is well known as a functional food due to its biological activities. Vascular calcification is associated with several disease conditions including atherosclerosis, diabetes, and chronic kidney disease (CKD), and is known to raise the risk of cardiovascular diseases related morbidity and mortality. However, there are no previous studies that have investigated the effects of fermented spinach exract (FSE) against aortic and its underlying mechanisms. Therefore, this study investigated the effects and action of possible mechanisms of FSE on inorganic phosphate (PI)-induced vascular calcification in ex vivo mouse aortic rings. PI increased vascular calcification through calcium deposition in ex vivo aortic rings. FSE inhibited calcium accumulation and osteogenic key marker, runt-related transcription factor 2 (Runx2), and bone Morphogenetic Protein 2 (BMP-2) protein expression in ex vivo aortic rings. And, FSE inhibited PI-induced extracellular signal-regulated kinase (ERK) and p38 phosphorylation in ex vivo aortic rings. These results show that FSE can prevent vascular calcification which may be a crucial way for the prevention and treatment of vascular disease association with vascular calcification.

Mitral Valve Replacement for Bulky, Calcified Mitral Annulus: A Case Report

  • Yusuke Nakata;Kazuyuki Miyamoto
    • Journal of Chest Surgery
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    • v.57 no.5
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    • pp.496-499
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    • 2024
  • Calcification of the mitral valve annulus is common in patients on dialysis. The growing number of individuals receiving dialysis has been accompanied by an increase in cases necessitating surgical intervention for mitral valve annulus calcification. In this report, we present a severe case characterized by bulky calcification of the mitral annulus, which was managed with mechanical mitral valve replacement. A 61-year-old man on dialysis presented with chest pain upon exertion that had persisted for 3 months. Cardiac echocardiography revealed severe mitral stenosis and regurgitation, accompanied by cardiac dysfunction. During surgery, an ultrasonic aspiration system was employed to remove the calcification of the mitral valve annulus to the necessary extent. Subsequently, a mechanical mitral valve was sutured into the supra-annular position. To address the regurgitation, the area surrounding the valve was sewn to the wall of the left atrium. Postoperative assessments indicated an absence of perivalvular leak and demonstrated improved cardiac function. The patient was discharged on postoperative day 22. We describe a successful mitral mechanical valve replacement in a case of extensive circumferential mitral annular calcification. Even with severe calcification extending into the left ventricular myocardium, we were able to minimize the decalcification process. This approach enabled the performance of mitral mechanical valve replacement in a high-risk patient on dialysis, thus expanding the possibilities for cardiac surgery.

Familial Idiopathic Basal Ganglia Calcification

  • Shin, Dong-Ah;Gong, Tae-Sik;Shin, Dong-Gyu;Kim, Hyoung-Ihl
    • Journal of Korean Neurosurgical Society
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    • v.40 no.3
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    • pp.196-198
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    • 2006
  • Familial idiopathic basal ganglia calcification[FIBGC] is an inheritable neurological condition characterized by calcium deposits in the basal ganglia and extra-basal ganglia areas. The condition manifests as parkinsonism and other variable neuropsychiatric symptoms. FIBGC is a rare condition, and its pathophysiology has not yet been fully elucidated. Here we report the results of a clinical study of two related patients diagnosed with FIBGC.