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Purpose@#Glabridin (GD) is a bio-available isoflavane isolated from the root extract of licorice (Glycyrrhiza glabra L.). It exhibits a variety of pharmacological activities such as antiinflammatory and anti-oxidant activities. However, extracellular vesicles (EVs) secretion and the anti-cancer mechanism of action remains largely unknown. The present study investigates the anticancer effects of GD by determining the inhibition of EVs secretion in the human breast cancer cell line, MDA-MB-231. @*Methods@#Cell viability, reactive oxygen species (ROS) production, migration, invasion rate, and vascular endothelial growth factor (VEGF) concentration were assessed in MDA-MB-231 cells treated with increasing concentrations of GD (0.1, 1, 5, 10, 20 μM). Subsequently, EV secretion and exosomal DEL-1 protein expression were evaluated to determine the anticancer effects of GD. @*Results@#The results showed that GD significantly inhibited the cell proliferation of MDAMB-231 cells in a dose- or time-dependent manner. Also, ROS production and apoptosis marker protein cleaved caspase-3 were significantly increased in GD-treated MDA-MB-231, compared to control. Furthermore, GD exposure resulted in significantly decreased not only migration and invasion rates but also the VEGF concentration, thereby contributing to a reduction in angiogenesis. Interestingly, the concentration and number of EVs as well as EV marker proteins, such as CD63 and TSG101, were decreased in GD-treated MDA-MB-231 cells. Markedly, extracellular matrix protein DEL-1 as angiogenesis factor was decreased in EVs from GD-treated MDA-MB-231 cells. @*Conclusion@#This study identifies that the anti-cancer molecular mechanism of GD is exerted via inhibition of angiogenesis and EVs secretion, indicating the potential of GD as a chemotherapeutic agent for breast cancer.
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Purpose@#Osteoporosis is characterized by structural deterioration of the bone tissue because of the loss of osteoblastic activity or the increase in osteoclastic activity, resulting in bone fragility and an increased risk of fractures. Hederagenin (Hed) is a pentacyclic triterpenoid saponin isolated from Dipsaci Radix, the dried root of Dipsacus asper Wall. Dipsaci Radix has been used in Korean herbal medicine to treat bone fractures. In this study, we attempted to demonstrate the potential anti-osteoporotic effect of Hed by examining its effect on osteoblast differentiation in MC3T3-E1 cells. @*Methods@#Osteoblastic MC3T3-E1 cells were cultured in 0, 1, and 10 μg/mL Hed for 3 and 7 days. The activity of alkaline phosphatase (ALP), bone nodule formation and level of expression of bone-related genes and proteins were measured in MC3T3-E1 cells exposed to Hed. The western blot test was used to detect the activation of the bone morphogenetic protein-2 (BMP2)/ Suppressor of Mothers against Decapentaplegic (SMAD)1 pathway. @*Results@#Hed significantly increased the proliferation of MC3T3-E1 cells. Intracellular ALP activity was significantly increased in the 1 μg/mL Hed-treated group. Hed significantly increased the concentration of calcified nodules. Furthermore, Hed significantly upregulated the expression of genes and proteins associated with osteoblast proliferation and differentiation, such as Runt-related transcription factor 2 (Runx2), ALP, osteopontin (OPN), and type I procollagen (ProCOL1). Induction of osteoblast differentiation by Hed was associated with increased BMP2. In addition, Hed induced osteoblast differentiation by increasing the activity of SMAD1/5/8. These results suggest that Hed has the potential to prevent osteoporosis by promoting osteoblastogenesis in osteoblastic MC3T3-E1 cells via the modulation of the BMP2/SMAD1 pathway. @*Conclusion@#The results presented in this study indicate that Hed isolated from Dipsaci Radix has the potential to be developed as a healthcare food and functional material possessing anti-osteoporosis effects.
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This report demonstrates a method of generating a chair-side and computer-aided template for implant surgery based on the Top-Down and restoration-driven concept. Compared to the traditional CAD-CAM process which requires multiple steps to be taken between dental clinic and laboratory, this alternative procedure, VARO guide system (VARO Guide, CAD, Pre-Guide, VARO-mill, NeoBiotech, Seoul, South Korea) enables accurate and patient-friendly implant surgery as well as immediate provisional restoration in a single visit. First, bite-registration at centric jaw relation and CBCT were taken using the Pre-Guide. The CBCT data was then reorganized directly through the chair-side CAD, and we could determine the most appropriate 3-dimensional position of implant. The STL file was extracted and put into the chair-side CAM (VARO-mill) to fabricate a VARO. This surgical guide allowed the implants to be accurately positioned into the planned sites within an hour.
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Purpose@#Zinc is known to be associated with osteoblast proliferation and differentiation.Osterix as zinc-finger transcription factor is also related to osteoblast differentiation and bone formation. In the present study, we aimed to investigate whether zinc modulates osterix gene and protein expression in osteoblastic MC3T3-E1 cells. @*Methods@#MC3T3-E1 cells were cultured in zinc-dependent concentrations (0, 0.5, 1, 5, or 15 µM Zn), along with osteogenic control (normal osteogenic medium) for 1 and 3 days. The gene and protein expression levels of osterix were analyzed by real-time reverse transcription polymerase chain reaction and Western blotting, respectively. @*Results@#Zinc increased osteoblast proliferation in a concentration-dependent manner at day 1 and 3. Similarly, zinc increased the activity of osteoblast marker enzyme alkaline phosphatase in cells and media in a zinc concentration-dependent manner. Moreover, our results showed that the pattern of osterix gene expression by zinc was down-regulated within the low levels of zinc treatments (0.5–1 µM) at day 1, but it was up-regulated after extended culture period at day 3. Osterix protein expression by zinc showed the similar pattern of gene expression, which down-regulated by low zinc levels at day 1 and up-regulated back at day 3 as the early stage of osteoblast differentiation. @*Conclusion@#Our results suggest that zinc modulates osterix gene and protein expression in osteoblasts, particularly in low level of zinc at early stage of osteoblast differentiation period.
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Purpose@#Corosolic acid (CA), also known as 2α-hydroxyursolic acid, is present in numerous plants, and is reported to exhibit anti-cancer and anti-proliferative activities in various cancer cells such as osteosarcoma, hepatocellular carcinoma, lung adenocarcinoma, and colon cancer. However, the anti-cancer activity of CA on human breast cancer cells and the underlying mechanisms remain to be elucidated. The present study aimed to investigate the anticancer effects of CA in the human breast cancer cell line, MDA-MB-231. @*Methods@#Cell viability, reactive oxygen species (ROS) production, apoptosis marker protein expression, migration, invasion rate, and vascular endothelial growth factor (VEGF) levels were assessed by treating MDA-MB-231 cells to increasing concentrations of CA. @*Results@#The results showed that CA significantly inhibited the cell proliferation of MDA-MB-231 cells in a dose-dependent manner. To assess the effect of CA on apoptosis, nuclei of MDA-MB-231 cells were stained with DAPI solution. Chromatin condensation, which indicates apoptosis, was observed to increase dose-dependently. In addition, western-blot analysis revealed elevated levels of the apoptosis marker proteins (Bax and cleaved caspase 3) subsequent to MDA-MB-231 exposure to CA. ROS production was also increased in the CA-induced apoptosis in MDA-MB-231 treated cells. Interestingly, CA exposure resulted in significantly decreased migration and invasion rates in the MDA-MB-231 cells. Data further revealed that exposure to CA markedly decreased the VEGF concentration, thereby contributing to a reduction in angiogenesis. @*Conclusion@#Our results determined that exposure to CA induces anti-proliferation, apoptosis, and ROS production, and suppresses cell migration and invasion rate in MDA-MB-231 cells. Taken together, these results indicate the potential of CA to be applied as an effective chemotherapeutic agent for treating breast cancer.
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Purpose@#Weight gain after kidney transplantation is a critical factor that can lead to poor outcomes with cardiovascular complications. Many studies have been conducted to identify predictive markers of future weight changes at the time of transplant. Recently, circulating exosomes and its contents including miRNAs and proteins have attracted attention as potential biomarkers. In this pilot study, we investigated exosomal proteins and weight change after kidney transplant. @*Methods@#Recipients (n=10) were classified into two groups; weight gainers (n=5, 9.7±4.4kg) and weight losers (n=5, -6.4±1.8kg) based on their weight changes at 12-months posttransplant. Based on the exosomal protein profiles obtained by the LC-MS/MS, differentially expressed proteins were identified between the groups. @*Results@#Concentration and the mean size of exosomes significantly increased at 12-months compared to the baseline (p=.009) in the total group. Eleven exosomal proteins were found at the baseline as differentially expressed between the two groups. In the weight gain group, complement proteins including HV169, C3, C4B, and C4A, were significantly upregulated. @*Conclusion@#Our pilot study suggests that exosomal complementary proteins are associated with weight gain after kidney transplantation. Further studies are needed to clarify the role of these exosomal proteins in the underlying mechanisms of weight changes in kidney transplant recipients.
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The use of an obturator prosthesis for patients with maxillary defects is a common treatment method to improve their oral function and achieve esthetic satisfaction. However, due to various difficulties and complexities, conventional methods for fabricating dental obturators continue to pose a challenge for dentists and patients, as well as laboratory technicians. CAD-CAM technologies may make it simple to fabricate maxillofacial prostheses including hollow obturators, which could improve comfort for clinicians by reducing burdensome manipulations. In addition, patients without a specialist in their vicinity will be able to be treated via cooperation between a nearby general practitioner and a distant prosthodontist. The aim of this clinical report is to investigate the possibility of using digitally fabricated maxillofacial prostheses that can be designed in one location, and manufactured in another in clinical situations.
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The purpose of this study is to compare the volume stability depending on the mixing methods and storage time for the conventional alginate and extended-pouralginate. Materials and methods: An arch-shaped metal model was fabricated, and one conventional alginate and two extended-pour alginates were used to take impressionsusing different mixing methods (hand and automatic). 120 impressions were taken (40 per each alginate) and stone models were made in accordance with the different storagetimes (immediate, 2 days, 5 days, and 6 days). The models were scanned with a 3D table scanner and dimensional change was measured by superimposing the scan data.Using SAS 9.4 (SAS Institute Inc., Cary, NC, USA), the general linear model and Tukey’s post hoc test was conducted for statistical analysis (P<.001). Results: There wasno statistically significant difference in the dimensional accuracy between two mixing methods, and the volume change was minimum when the stone was poured immediatelyin all groups. Dimensional accuracy showed a statistically significant difference between groups after 2 days of storage, and extended-pour alginate showed higher accuracyafter 5 days of storage comparing to conventional one. Large amounts of volume change were showed at 2 - 5 days for conventional alginate and at 5 - 6 days forextended pour alginate. Conclusion: The mixing method of alginate does not affect volume stability. Although extended-pour alginate has better volume stability than conventionalalginate for a long time, it is recommended to pour stone as soon as possible. (J Korean Acad Prosthodont 2020;58:86-94)
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Purpose@#The vascular smooth muscle cells (VSMCs) in mature animals have implicated to play a major role in the progression of cardiovascular diseases such as atherosclerosis. This study aimed at optimizing the protocol in culturing primary VSMCs (pVSMCs) from rat thoracic aorta and investigating the effect of cellular zinc (Zn) deficiency on cell proliferation of the isolated pVSMCs. @*Methods@#The thoracic aorta from 7-month-old Sprague Dawley rats was isolated, minced and digested by the enzymatic process of collagenase I and elastase, and then inoculated with the culture Dulbecco Modified Eagle Medium (DMEM) at 37°C in an incubator. The primary cell culture morphology was observed using phase-contrast microscopy and cellular Zn was depleted using Chelex-100 resin (extracellular zinc depletion only) or 3 µM N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN) (extracellular and intracellular zinc depletion). Western blot analysis was used for the detection of SM22α and calponin as smooth muscle cell marker proteins and von Willebrand factor as endothelial cell marker protein to detect the culture purity. Cell proliferation by Zn depletion (1 day) was measured by MTT assay. @*Results@#A primary culture protocol for pVSMCs from rat thoracic aorta was developed and optimized. Isolated cultures exhibited hill and valley morphology as the major characteristics of pVSMCs and expressed the smooth muscle cell protein markers, SM22α and calponin, while the endothelial marker von Willebrand factor was hardly detected. Zn deprivation for 1 day culture decreased rat primary vascular smooth muscle cell proliferation and this pattern was more prominent under severe Zn depletion (3 µM TPEN), while less prominent under mild Zn depletion (Chelexing). @*Conclusion@#Our results suggest that cellular Zn deprivation decreased pVSMC proliferation and this may be involved in phenotypic modulation of pVSMC in the aorta.
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Purpose@#The vascular smooth muscle cells (VSMCs) in mature animals have implicated to play a major role in the progression of cardiovascular diseases such as atherosclerosis. This study aimed at optimizing the protocol in culturing primary VSMCs (pVSMCs) from rat thoracic aorta and investigating the effect of cellular zinc (Zn) deficiency on cell proliferation of the isolated pVSMCs. @*Methods@#The thoracic aorta from 7-month-old Sprague Dawley rats was isolated, minced and digested by the enzymatic process of collagenase I and elastase, and then inoculated with the culture Dulbecco Modified Eagle Medium (DMEM) at 37°C in an incubator. The primary cell culture morphology was observed using phase-contrast microscopy and cellular Zn was depleted using Chelex-100 resin (extracellular zinc depletion only) or 3 µM N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN) (extracellular and intracellular zinc depletion). Western blot analysis was used for the detection of SM22α and calponin as smooth muscle cell marker proteins and von Willebrand factor as endothelial cell marker protein to detect the culture purity. Cell proliferation by Zn depletion (1 day) was measured by MTT assay. @*Results@#A primary culture protocol for pVSMCs from rat thoracic aorta was developed and optimized. Isolated cultures exhibited hill and valley morphology as the major characteristics of pVSMCs and expressed the smooth muscle cell protein markers, SM22α and calponin, while the endothelial marker von Willebrand factor was hardly detected. Zn deprivation for 1 day culture decreased rat primary vascular smooth muscle cell proliferation and this pattern was more prominent under severe Zn depletion (3 µM TPEN), while less prominent under mild Zn depletion (Chelexing). @*Conclusion@#Our results suggest that cellular Zn deprivation decreased pVSMC proliferation and this may be involved in phenotypic modulation of pVSMC in the aorta.
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Peri-implantitis appears in almost 20% of patients who received implant treatment, and increase in its number is inevitable as time goes by. Although it can be treated by both non-surgical and surgical procedures, in cases which include severe bone loss, explantation and rehabilitation may be necessary. Careful treatment planning and considerations to prevent recurrent peri-implantitis should be taken into account. In the following case presented, a patient with chronic periodontitis and peri-implantitis was successfully rehabilitated after removal of several implants. Extraction and explantation of multiple teeth and implants were followed by full mouth reconstruction with fixed implant prostheses on the mandible and implant retained overdenture on the maxilla. Surgical and prosthetic measures to prevent recurrent peri-implantitis were taken into consideration.
Subject(s)
Humans , Chronic Periodontitis , Denture, Overlay , Mandible , Maxilla , Mouth Rehabilitation , Mouth , Peri-Implantitis , Prostheses and Implants , Rehabilitation , ToothABSTRACT
PURPOSE: Runx2 (runt-related transcription factor 2), a bone-specific transcription factor, is a key regulator of osteoblast differentiation and its expression is induced by the activation of BMP-2 signaling. This study examined whether zinc modulates BMP-2 signaling and therefore stimulates Runx2 and osteoblast differentiation gene expression. METHODS: Two osteoblastic MC3T3-E1 cell lines (subclones 4 as a high osteoblast differentiation and subclone 24 as a low osteoblastic differentiation) were cultured in an osteogenic medium (OSM) as the normal control, Zn− (1 µM Zn) or Zn+ (15 µM Zn) for 24 h. The genes and proteins for BMP-2 signaling (BMP-2, Smad-1/p-Smad-1), transcription factors (Runx2, osterix), and osteoblast differentiation marker proteins were assessed. RESULTS: In both cell lines, BMP-2 mRAN and protein expression and extracellular BMP-2 secretion all decreased in Zn−. The expression of Smad-1 (downstream regulator of BMP-2 signaling) and p-Smad-1 (phosphorylated Smad-1) also downregulated in Zn−. Furthermore, the expression of the bone-specific transcription factors, Runx2 and osterix, decreased in Zn−, which might be due to the decreased BMP-2 expression and Smad-1 activation (p-Smad-1) by Zn−, because Runx2 and osterix both are downstream in BMP-2 signaling. Bone marker gene expression, such as alkaline phosphatase (ALP), collagen type I (COLI), osteocalcin, and osteopontin were also downregulated in Zn−. CONCLUSION: The results suggest that a zinc deficiency in osteoblasts suppresses the BMP-2 signaling pathway via the suppression of Smad-1 activation, and this suppressed BMP-2 signaling can cause poor osteoblast differentiation.
Subject(s)
Alkaline Phosphatase , Cell Line , Collagen Type I , Gene Expression , Osteoblasts , Osteocalcin , Osteopontin , Phosphorylation , Transcription Factors , ZincABSTRACT
BACKGROUND: This study was conducted to evaluate the impact of the media type used for direct identification of colonies on the surveillance culture of carbapenem-resistant Enterobacteriaceae (CRE) by matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS). METHODS: CRE surveillance culture isolates were subjected to species identification using the MALDI Biotyper (Bruker Daltonics, Germany) for 2 months starting in March 2017. Four types of media were evaluated: blood agar (BA), Mueller Hinton agar (MH), MacConkey agar (Mac), and MacConkey agar containing imipenem of 1 µg/mL (IMP-Mac). CRE-like colonies on IMP-Mac and their subculture colonies on the other media were tested after overnight incubation and extended incubation for one additional day. The percent identification and score value were analyzed for each media types and incubation time when the identification was correct at the genus level. RESULTS: A total of 117 isolates were identified as 84 Klebsiella pneumoniae, 12 Escherichia coli, 9 Enterobacter cloacae, 5 Klebsiella oxytoca, 4 Enterobacter aerogenes, and 2 Raoultella ornithinolytica. The successful identification rates (SIR) for BA and MH were 98.3% and 97.4% (P=0.9), respectively, while those for Mac and IMP-Mac were 82.1% (P < 0.001) and 70.9% (P < 0.001), respectively. After extended incubation, SIRs were decreased to 96.6%, 96.6% (P=1.0), 61.5% (P < 0.001), and 58.1% (P < 0.001) on BA, MH, Mac, and IMP-Mac, respectively. The average score values were significantly lower for Mac (2.017±0.22) and IMP-Mac (1.978±0.24) than for BA (2.213±0.16) (P < 0.001). CONCLUSIONS: The low performance of the MALDI Biotyper applied directly to the colonies grown on Mac or IMP-Mac indicates that subculture on BA or MH is preferable before identification by MALDI-TOF MS.
Subject(s)
Agar , Enterobacter aerogenes , Enterobacter cloacae , Enterobacteriaceae , Escherichia coli , Imipenem , Klebsiella oxytoca , Klebsiella pneumoniae , Mass Spectrometry , Spectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationABSTRACT
PURPOSE: The Glycyrrhiza uralensis species (Leguminosae) as a medicinal biocompound, and one of its root components, isoliquritigenin (ISL), which is a flavonoid, has been reported to have anti-tumor activity in vitro and in vivo. However, its function in bone formation has not been studied yet. In this study, we tested the effect of Glycyrrhiza uralensis (ErLR) and baked Glycyrrhiza uralensis (EdLR) extracts on osteoblast proliferation, alkaline phosphatase (ALP) activity, and bone-related gene expression in osteoblastic MC3T3-E1 cells. METHODS: MC3T3-E1 cells were cultured in various levels of ErLR (0, 5, 10, 15, 20 µg/mL), EdLR (0, 5, 10, 15, 20 µg/mL), or ISL (0, 5, 10, 15, 20 µM) in time sequences (1, 5, and 20 days). Also, isoliquritigenin (ISL) was tested for comparison to those two biocompound extracts. RESULTS: MTT assay results showed that all three compounds (ErLR, EdLR, and ISL) increased osteoblastic-cell proliferation in a concentration-dependent manner for one day. In addition, both ErLR and EdLR compounds elevated the osteoblast proliferation for 5 or 20 days. Extracellular ALP activity was also increased as ErLR, EdLR, and ISL concentration increased at 20 days, which implies the positive effect of Glycyrrhiza species on osteoblast mineralization. The bone-related marker mRNAs were upregulated in the ErLR-treated osteoblastic MC3T3-E1 cells for 20 days. Bone-specific transcription factor Runx2 gene expression was also elevated in the ErLR- and EdLR-treated osteoblastic MC3T3-E1 cells for 20 days. CONCLUSION: These results demonstrated that Glycyrrhiza uralensis extracts may be useful for preventing osteoporosis by increasing cell proliferation, ALP activity, and bone-marker gene expression in osteoblastic cells.
Subject(s)
Alkaline Phosphatase , Cell Proliferation , Gene Expression , Glycyrrhiza uralensis , Glycyrrhiza , In Vitro Techniques , Miners , Osteoblasts , Osteogenesis , Osteoporosis , RNA, Messenger , Transcription FactorsABSTRACT
PURPOSE: Zinc (Zn) is an essential trace element for bone mineralization and osteoblast function. We examined the effects of Zn deficiency on osteoblast differentiation and mineralization in MC3T3-E1 cells. METHODS: Osteoblastic MC3T3-E1 cells were cultured at concentration of 1 to 15 µM ZnCl2 (Zn− or Zn+) for 5, 15 and 25 days up to the calcification period. Extracellular matrix mineralization was detected by staining Ca and P deposits using Alizarin Red and von Kossa stain respectively, and alkaline phosphatase (ALP) activity was detected by ALP staining and colorimetric method. RESULTS: Extracellular matrix mineralization was decreased in Zn deficiency over 5, 15, and 25 days. Similarly, staining of ALP activity as the sign of an osteoblast differentiation, was also decreased by Zn deficiency over the same period. Interestingly, the gene expression of bone-related markers (ALP, PTHR; parathyroid hormone receptor, OPN; osteopontin, OC; osteocalcin and COLI; collagen type I), and bone-specific transcription factor Runx2 were downregulated by Zn deficiency for 5 or 15 days, however, this was restored at 25 days. CONCLUSION: Our data suggests that Zn deficiency inhibits osteoblast differentiation by retarding bone marker gene expression and also inhibits bone mineralization by decreasing Ca/P deposition as well as ALP activity.
Subject(s)
Alkaline Phosphatase , Calcification, Physiologic , Collagen , Extracellular Matrix , Gene Expression , Methods , Miners , Osteoblasts , Osteocalcin , Osteopontin , Receptor, Parathyroid Hormone, Type 1 , Transcription Factors , ZincABSTRACT
This study was performed to evaluate whether microRNAs (miRNAs) in circulating exosomes may serve as biomarkers of drug-induced liver, kidney, or muscle-injury. Quantitative PCR analyses were performed to measure the amounts of liver-specific miRNAs (miR-122, miR-192, and miR-155), kidney-specific miR-146a, or muscle-specific miR-206 in plasma and exosomes from mice treated with liver, kidney or muscle toxicants. The levels of liver-specific miRNAs in circulating plasma and exosomes were elevated in acetaminophen-induced liver injury and returned to basal levels by treatment with antioxidant N-acetyl-cysteine. Circulating miR-146a and miR-206 were increased in cisplatin-induced nephrotoxicity and bupivacaine-induced myotoxicity, respectively. Taken together, these results indicate that circulating plasma and exosomal miRNAs can be used as potential biomarkers specific for drug-induced liver, kidney or muscle injury.
Subject(s)
Animals , Mice , Biomarkers , Exosomes , Kidney , Liver , MicroRNAs , Plasma , Polymerase Chain Reaction , RodentiaABSTRACT
This study was performed to evaluate whether microRNAs (miRNAs) in circulating exosomes may serve as biomarkers of drug-induced liver, kidney, or muscle-injury. Quantitative PCR analyses were performed to measure the amounts of liver-specific miRNAs (miR-122, miR-192, and miR-155), kidney-specific miR-146a, or muscle-specific miR-206 in plasma and exosomes from mice treated with liver, kidney or muscle toxicants. The levels of liver-specific miRNAs in circulating plasma and exosomes were elevated in acetaminophen-induced liver injury and returned to basal levels by treatment with antioxidant N-acetyl-cysteine. Circulating miR-146a and miR-206 were increased in cisplatin-induced nephrotoxicity and bupivacaine-induced myotoxicity, respectively. Taken together, these results indicate that circulating plasma and exosomal miRNAs can be used as potential biomarkers specific for drug-induced liver, kidney or muscle injury.
Subject(s)
Animals , Mice , Biomarkers , Exosomes , Kidney , Liver , MicroRNAs , Plasma , Polymerase Chain Reaction , RodentiaABSTRACT
In implant restorations, it is difficult for the patient to percept any symptoms. In addition, they are absent of shock absorbers, which can lead to mechanical failure if stress distribution is not considered. Since maxillary anterior multiple-implant restorations play a significant role in guiding the functional movement of the mandible by distributing lateral force, it is crucial to form appropriate occlusion. The use of the T-scan system is more advantageous in assessing ‘dynamic occlusion’, such as the change of occlusion over time, the amount of tooth contact during functional movement, and assessing the occlusion in the less-visible posterior teeth. The case is reported as it has satisfactory results in harmonious anterior guidance of a maxillary anterior multiple-implant restoration using T-scan analysis.
Subject(s)
Humans , Mandible , Prostheses and Implants , Shock , ToothABSTRACT
Zinc is an essential trace element required for bone formation, however not much has been clarified yet for its role in osteoblast. We hypothesized that zinc would increase osteogenetic function in osteoblasts. To test this, we investigated whether zinc treatment enhances bone formation by stimulating osteoblast proliferation, bone marker protein alkaline phosphatase activity and collagen synthesis in osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were cultured and treated with various concentrations of zinc (0, 1, 3, 15, 25 uM) along with a normal osteogenic medium (OSM) as control for 1, 5, 10 days. As measured by MTT assay for mitochondrial metabolic activity, cell proliferation was stimulated even at low zinc treatment (1-3 micrometer) compared to OSM, and it was stimulated in a zinc concentration-dependent manner during 5 and 10 days, with the most pronounced effect at 15 and 25 uM Zn. Cellular (synthesized) alkaline phosphatase (ALP) activity was increased in a zinc concentration-dependent manner, so did medium (secreted) ALP activity. Cellular collagen concentration was increased by zinc as time went by, therefore with the maximum zinc stimulatory effect in 10 days, and medium collagen concentration showed the same pattern even on 1 and 5 day. This zinc stimulatory effect of collagen synthesis was observed in cell matrix collagen staining. The study results imply that zinc can increase osteogenic effect by stimulating cell proliferation, ALP activity and collagen synthesis in osteoblastic cells.
Subject(s)
Alkaline Phosphatase , Cell Proliferation , Collagen , Durapatite , Osteoblasts , Osteogenesis , ZincABSTRACT
Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with TNFalpha for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy (15 micrometer Zn) or Zn-deficiency (0 micrometer Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various TNFalpha (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, 0-30 microM) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-alpha treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-alpha and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.