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9 publications mentioning hsa-mir-634

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-634. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 234
Moreover, the inhibitory effect of the overexpression of miR-634 on cell survival in cancer cells has already been demonstrated: that the overexpression of miR-634 activates the mitochondrial apoptotic pathway by direct concurrent targeting of genes associated with mitochondrial homeostasis, anti-apoptosis, antioxidant ability and autophagy in a mo del of esophageal squamous cell carcinoma 35, and that miR-634 is one of the most effective miRNAs to induce apoptosis and inhibit the level of p-Akt in HER2 positive breast cancer 36. [score:12]
The results of Fig. 4(c) displayed that miR-634 mimic down-regulated the mRNA level of p85α, while miR-634 inhibitor up-regulated the mRNA level of p85α (Fig. 4(c), *P < 0.05, ***P < 0.001, versus NC). [score:9]
Here, our findings that the overexpression of miR-634 suppressed the phosphorylation of Akt indicated that miR-634 exerted an inhibitory effect on the PI3K/Akt pathway by targeting PIK3R1 gene. [score:9]
Therefore, the overexpression of miR-634 could inhibit cell survival and matrix synthesis by targeting PIK3R1 to modulate PI3K/Akt signal cascade in high grade OA chondrocytes. [score:7]
How to cite this article: Xu, C. et al. Overexpression of microRNA-634 suppresses survival and matrix synthesis of human osteoarthritis chondrocytes by targeting PIK3R1. [score:7]
Diana-MICROT, miRDB, TargetMiner, and TargetScan, were chosen to determine the possible target genes of miR-634. [score:7]
Moreover, the results of ELISA showed that the variation tendency of MMP13 protein expression in extracellular matrix of OA chondrocytes transfected with mimic or inhibitor of miR-634 (the right panel in Fig. 2(c,d), *P < 0.05, ***P < 0.001) was in accordance with that of intracellular MMP13 protein expression (the left & middle panel in Fig. 2(c,d)). [score:7]
The results showed that miR-634 could down-regulate the luciferase activity of pmiR-PIK3R1-WT plasmid, but not that of pmiR-PIK3R1-MUT, manifesting that PIK3R1 was one of miR-634 targets (Fig. 4(b), ***P < 0.001, versus NC). [score:6]
Similarly, miR-634 mimic down-regulated the protein level of p85α (Fig. 4(d), *P < 0.05, versus NC) and vice versa in OA chondrocytes transfected with miR-634 inhibitor (Fig. 4(e), ***P < 0.001, versus NC). [score:6]
In conclusion, we demonstrated that miR-634 was expressed differentially in the whole OA pathological progression, including higher expression in low grade OA chondrocytes and lower expression in high grade OA chondrocytes, compared with normal chondrocytes. [score:6]
Consequently, miR-634 could regulate the mRNA and protein level of p85α, indicating that PIK3R1 could be one of target genes inhibited by miR-634 in high grade OA chondrocytes. [score:6]
However, miR-634 inhibitor up-regulated the mRNA levels of COL2A1 and ACNA without the alteration of ADAMTS-5 and MMP13 in mRNA levels (Fig. 2(b), *P < 0.05, ***P < 0.001, versus NC). [score:6]
Therefore, miR-634 could target PIK3R1 to inhibit the PI3K/Akt/S6 and PI3K/Akt/mTOR/S6 axes, contributing to the regulatory mechanism of miR-634 on survival and matrix metabolism in high grade OA chondrocytes. [score:6]
These results suggested that the overexpression of miR-634 has an inhibitory effect on the PI3K/Akt pathway, partly associated with mTOR and S6 signal molecules. [score:5]
Together, the data indicated that the overexpression of miR-634 could suppress matrix synthesis in high grade OA chondrocytes. [score:5]
Overall, the overexpression of miR-634 could inhibit survival of high grade OA chondrocytes. [score:5]
Neither miR-634 mimic nor miR-634 inhibitor had effect on ADAMTS-5 protein expression. [score:5]
Based on bioinformatics prediction, our results of dual-luciferase and qPCR analysis gave evidence that miR-634 could bind to the complementary sequences in the 3′UTR of PIK3R1 gene, and inhibit PIK3R1mRNA expression in OA chondrocytes. [score:5]
Overexpression of miR-634 could suppress cell survival and matrix synthesis in high grade OA chondrocytes. [score:5]
Therefore, we suggested that PIK3R1 is one of the putative target genes inhibited by miR-634. [score:5]
Furthermore, miR-634 targeted PIK3R1 gene that encodes the regulatory subunit 1 of class I PI3K (p85α) followed by the regulation of the PI3K/Akt/S6 and PI3K/Akt/mTOR/S6 axes in high grade OA chondrocytes. [score:5]
However, our data indicated that decreased miR-634 exerted the inhibitory effect on survival and matrix synthesis in high grade OA chondrocytes, seeming to be contrary to conventional deduction that only the higher expressed elements could have an effect on cell events. [score:5]
Additionally, the released concentrations of GAGs that is a vital component of extracellular matrix declined in OA chondrocytes transfected with miR-634 mimic, while miR-634 inhibitor up-regulated the released concentrations of GAGs using DMMB assay (Fig. 2(e), **P < 0.01, versus NC), similar to the variation tendency of AGG using western blotting analysis (Fig. 2(c,d)). [score:5]
Consistent with these studies, our findings of the effect of miR-634 on the phosphorylation of mTOR and S6 is indicative of the involvement of the PI3K/Akt/S6 (miR-634 mimic) and PI3K/Akt/mTOR/S6 (miR-634 inhibitor) axes in the regulatory mechanism of miR-634. [score:4]
The results of qPCR showed that miR-634 mimic dramatically down-regulated the mRNA levels of COL2A1 and ACNA, while the mRNA levels of ADAMTS-5 and MMP13 increased (Fig. 2(a), **P < 0.01, ***P < 0.001, versus NC). [score:4]
Amongst the 7 miRNAs (miR-483-5p, miR-149, miR-582-3p, miR-1227, miR-634, miR-576-5p, and miR-641) detected by Silvia Díaz-Prado1 et al., 6 miRNAs were down-regulated in OA chondrocytes, and miR-634 is one of the six miRNAs 16. [score:4]
Based on our data of the high expression of miR-634 in low grade OA chondrocytes, we speculate that the increase of miR-634 may contribute to the development of OA pathogenesis. [score:4]
Here, our data also indicated that miR-634 could regulate the expression of main biological markers in matrix metabolism, such as Col II, AGG, MMP13, and ADAMTS-5 in high grade OA chondrocytes. [score:4]
Consistent with the above study, our data indicated the down-regulation of miR-634 in high grade OA chondrocyte compared with normal chondrocytes. [score:3]
The miR-634 target region of the PIK3R1-3′UTR was inserted into the pmiR-RB-Report vector and named pmiR-PIK3R1-WT (RiboBio, Guangzhou, China). [score:3]
As a control, the plasmid containing the mutant sequence of the miR-634 target region of the PIK3R1 3′UTR was also inserted into the pmiR-RB-Report vector and named pmiR-PIK3R1-MUT. [score:3]
After high grade OA chondrocytes were transfected with miR-634 mimic, miR-634 inhibitor, and their negative control (NC) for 48~96 h, respectively, the mRNA/protein levels of matrix synthesis biomarkers, including COL2A1/Col II, ACNA/AGG, ADAMTS-5/ADAMTS-5, and MMP13/MMP13, were detected using technique and western blotting analysis, respectively. [score:3]
These findings could support our data that miR-634 suppressed survival of OA chondrocytes. [score:3]
To investigate whether miR-634 has an inhibitory effect on the PI3K/Akt pathway, cells were transfected with miR-634 mimic, miR-634 inhibitor or their negative control in OA chondrocytes, respectively. [score:3]
To determine whether miR-634 could target PIK3R1, HEK293 cells were transiently co -transfected with the pmiR-PIK3R1-WT (wild-type 3′UTR) or pmiR-PIK3R1-MUT (mutant sites) of PIK3R1 REPORT™ reporter plasmids, and miR-634 mimic, respectively, prior to dual-luciferase analysis. [score:3]
The expression of miR-634 in human normal and OA chondrocytes. [score:3]
In contrast, miR-634 inhibitor promoted cell proliferation of OA chondrocyte at the same time (Fig. 3(b), *P < 0.05, versus NC). [score:3]
Cells were transfected with miR-634 mimic or miR-634 inhibitor and their negative control for 48~96 h, respectively. [score:3]
Meanwhile, the protein level of Bcl-2 decreased in OA chondrocytes transfected with miR-634 mimic (Fig. 3(c), ***P < 0.001, versus NC) and vice versa in OA chondrocytes transfected with miR-634 inhibitor (and 3(d), **P < 0.01, versus NC). [score:3]
org) were used to predict the miR-634 targets. [score:3]
Human chondrocytes were transfected with miR-634 mimic or miR-634 inhibitor (Ribobio, Guangzhou, China) at 30 nM or 200 nM, respectively, using Lipofectamine 3000 according to the manufacturer’s protocol (Invitrogen, USA). [score:3]
Therefore, it is confirmed that miR-634 is expressed at the lower level in high grade OA chondrocytes. [score:3]
Meanwhile, the level of p-Akt, p-mTOR, and p-S6 increased in OA chondrocytes transfected with miR-634 inhibitor, while total Akt and mTOR did not change (Fig. 5(b), *P < 0.05, **P < 0.01, versus NC). [score:3]
Hence, we suggested that miR-634 could be involved in regulating survival and matrix synthesis of OA chondrocytes. [score:2]
The results of CCK8 assay showed that miR-634 mimic inhibited cell proliferation of OA chondrocyte at the 9 [th] day (Fig. 3(a), *P < 0.05, versus NC). [score:2]
Meanwhile, miR-634 was involved in regulating chondrocyte survival, similar to the effect of other miRNAs on chondrocyte survival. [score:2]
Whereas, the decrease of miR-634 in high grade OA chondrocytes may be attributed to a spontaneous resistance of chondrocytes to OA pathological microenvironment, or more complicate regulatory mechanism on miR-634. [score:2]
It was found that 3′UTR of PIK3R1, which encodes class I PI3K regulatory subunit 1 (α) (PIK3R1, alias: p85-α) 21, contained the miR-634 seed sites and that sequences were highly conserved among diverse species (Fig. 4(a)). [score:2]
MiR-634 targets PIK3R1 in human OA chondrocytes. [score:2]
MiR-634 inhibitor led to the increase in AGG and Col II protein levels with the decrease of MMP13 protein level (the left panel in Fig. 2(d), **P < 0.01, ***P < 0.001, versus NC). [score:2]
The effect of miR-634 on survival of human OA chondrocytes. [score:1]
The gene expression of microRNA-634 was measured using qPCR technique as described in the. [score:1]
The effect of miR-634 on the PI3K/Akt pathway in human OA chondrocytes. [score:1]
The role of miR-634 in the whole OA progression needs to be further studied. [score:1]
The effect of miR-634 on matrix synthesis of human OA chondrocytes. [score:1]
The results of western analysis manifested that the protein levels of AGG and Col II decreased, with the increase in MMP13 protein level in OA chondrocytes transfected with miR-634 mimic (the left & middle panel in Fig. 2(c), **P < 0.01, ***P < 0.001, versus NC). [score:1]
HEK293 cells were transiently co -transfected with the 100 ng pmiR-PIK3R1-WT or pmiR-PIK3R1-MUT and 30 nM miR-634 mimic or its negative control using Lipofectamine 3000 (Invitrogen, CA, USA) in 24-well plates, respectively. [score:1]
As showed in Fig. 5(a), miR-634 reduced the levels of p-Akt and p-S6 without the alteration of Akt, mTOR and p-mTOR levels ([*]P < 0.05, ***P < 0.001, versus NC). [score:1]
As shown in Fig. 1, the gene level of miR-634 in Moderate and Severe group was the lowest in the three groups, while the gene level of miR-634 in Mild group was the highest in the three groups (Fig. 1, *P < 0.05, ***P < 0.001). [score:1]
Cells were transfected with miR-634 mimic, miR-634 inhibitor or their negative control for 72 h or 96 h, and then the levels of Akt, p-Akt, mTOR, p-mTOR, p-S6, and GAPDH were measured by western blotting analysis using Akt(1:2000), p-Akt(1:1500), mTOR(1:2000), p-mTOR (1:2000), p-S6(1:2000), and GAPDH(1:20000) antibodies under the same experimental conditions (8% or 10% SDS-PAGE) as described in the. [score:1]
Modulation of miR-634 on the PI3K/Akt pathway. [score:1]
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2
[+] score: 33
Amongst these 7 human miRNAs, 1 was up-regulated in OA chondrocytes (hsa-miR-483-5p) and 6 were up-regulated in normal chondrocytes (hsa-miR-149*, hsa-miR-582-3p, hsa-miR-1227, hsa-miR-634, hsa-miR-576-5p and hsa-miR-641). [score:7]
Amongst these 7 human miRNAs, 1 was up-regulated in OA chondrocytes (hsa-miR-483-5p) and 6 were up-regulated in normal chondrocytes in comparison to OA chondrocytes (hsa-miR-149*, hsa-miR-582-3p, hsa-miR-1227, hsa-miR-634, hsa-miR-576-5p and hsa-miR-641) (Figure 2 B and C). [score:7]
The number of transcription proteins obtained as putative mRNA targets regulated by hsa-miR-145, hsa-miR-576-5p and hsa-miR-1227 were also high (18% to 19%), whereas secretory, membrane, surface or receptor proteins as predicted targets regulated by hsa-miR-149, hsa-miR-483-5p, hsa-miR-582-3p, hsa-miR-634 and hsa-miR-641 were also elevated (15 to 19%). [score:7]
It is noteworthy that some of the miRNAs differentially expressed in chondrocyte that we identified in our study are novel as compared with those identified and published in the literature, e. g. hsa-miR-576-5p, hsa-miR-582-3p, hsa-miR-634, hsa-miR-641, hsa-miR-1227, suggesting that they may therefore represent new targets in articular cartilage. [score:4]
On the other hand, hsa-miR-582-3p, hsa-miR-641, hsa-miR-149 and hsa-miR634 were down-regulated in OA chondrocyte micropellets, 3.9, 1.52, 2.6 and 4.03 fold respectively, in agreement with data, although there were no statistical significant differences when comparing the different miRNA R. E. L. in normal versus OA chondrocyte micropellets (p > 0.05, U Mann–Whitney test). [score:4]
We selected the hsa-miR-149, hsa-miR-483-5p, hsa-miR-582-3p, hsa-miR-634 and hsa-miR-641 differentially expressed for further quantification using quantitative PCR techniques (Figure 4). [score:3]
PCR amplification of microRNAs (hsa-miR-145, hsa-miR-149, hsa-miR-483-5p, hsa-miR-582-3p, hsa-miR-634 and hsa-miR-641; as annotated in the miRBase ver 10.0 and 11.0) was carried out on the LightCycler® 480 Instrument (Roche, Mannheim, Germany) using miRCURY LNA [TM] microRNA PCR System (Exiqon, Vedbaek, Denmark). [score:1]
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3
[+] score: 13
Cui X. Wang S. Cai H. Lin Y. Zheng X. Zhang B. Xia C. Overexpression of microRNA-634 suppresses survival and matrix synthesis of human osteoarthritis chondrocytes by targeting PIK3R1 Sci. [score:7]
A microarray -based, large-scale analysis identified the signatures of six miRNA, of which levels are increased in normal chondrocytes of human origin relative to OA chondrocytes (miRNA-1227, miRNA-576-5p, miRNA-149*, miRNA-634, miRNA-641, and miRNA-582-3p) and a single miRNA, namely miRNA-483-5p, which is selectively up-regulated in OA chondrocytes [108]. [score:4]
Noticeably, miRNA mimics have been used to uncover the role of the miRNA-30b/ERG pathway in OA [140], as well as the regulatory function of miRNA-634 in chondrocyte metabolism [141]. [score:2]
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4
[+] score: 12
The expression levels of miR-17-5p, miR-593, miR-23a-5p, miR-586, miR-1180, miR-508-5p, miR-511, miR-646, miR-634, miR-149-5p, miR-24-3p, miR-1267, miR-504 and miR-1270 were upregulated. [score:6]
The expression levels of miR-17-5p, miR-593, miR-23a-5p, miR-586, miR-1180, miR-508-5p, miR-511, miR-646, miR-634, miR-149-5p, miR-24-3p, miR-1267, miR-504 and miR-1270 were upregulated (Fig. 2A) (P<0.05). [score:6]
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5
[+] score: 10
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
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6
[+] score: 5
[44] Bach et al. [45] identified eight miRNAs that were significantly differentially expressed 5 h after PDT, compared with baseline levels, and an up to 15-fold transient upregulation of miR-634, -1246 and -1290 relative to their basal levels. [score:5]
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[+] score: 5
miRNA miR function Regulation Tissue/cell type Source miR-16 p53, cell cycle, JAK/STAT signaling Down Placenta Maccani et al. 2010 miR-21 Fatty acid synthesis, apoptosis miR-146a Inflammation, NFκβ mediator miR-223 Immunology Up Maternal and cord blood Herberth et al. 2013 miR-129 Cell cycle regulation, apoptosis Down Spermatozoa Marczylo et al. 2012 miR-634 Inflammation miR-340 Cell migration and invasion Up Spermatozoa Marczylo et al. 2012 miR-365Targets NKX2.1 miR-143 Cardiogenesis Down Gastric tissue Stánitz et al. 2013 miR-21 Fatty acid biosynthesis, apoptosis Up Gastric tissue Stánitz et al. 2013 Let-7c Cell proliferation, angiogenesis Down Induced sputum Van Pottelberge et al. 2011 miR-146a Inflammation, NFκβ mediator miR-150 Hematopoeiesis miR-203 DNA damage response miR-340 Cell migration and invasion miR-443 Unknown miR-223 Immunology Down Plasma MV Badrnya et al. 2014 miR-29b Apoptosis Up Plasma MV Badrnya et al. 2014 RNU6-2 Reference miR MV, microvesicles. [score:5]
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8
[+] score: 4
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Indeed, although CTNNA2 can be regulated by primate-specific miRNAs common to both monkeys and humans (miR-513a-3p, miR-518a-5p, miR-548a-5p, miR-576-5p, miR-586, miR-607, miR-625, miR-642), a number of miRNAs present in Homo sapiens but not in Macaca mulatta (miR-1208, miR-1247, miR-1290, miR-1324, miR-1825, miR-613 and miR-634) also target CTNNA2 [19], [29]. [score:4]
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9
[+] score: 3
Among these miRNAs, only the expression of miR-634 correlated to our previous report on stroke with pre-existing risk factors [15]. [score:3]
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