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Calcibiotic Root Canal Sealer

Calcibiotic Root Canal Sealers are a class of dental materials used to fill and seal the inner chamber (root canal) of a tooth after the pulp (soft inner tissue) has been removed.
These sealers are designed to promote the healing and regeneration of the surrounding bone and tissues, while also providing a secure seal to prevent bacterial infection.
Key characteristics of Calcibiotic Root Canal Sealers include their biocermaic composition, antimicrobial properties, and ability to stimulate the formation of new bone.
Thier use is critical in endodontic (root canal) procedures to ensrue long-term tooth health and function.
Reasearchers can leverage PubCompare.ai to streamline their evaluations of different Calcibiotic Root Canal Sealer formulations and protocols, accelerating discoveries in this important area of dental sciene.

Most cited protocols related to «Calcibiotic Root Canal Sealer»

1
Comparative Gene Expression Profiling of Colorectal Cancer Stages
Consistent gene expression changes were identified between 44 stage A and 61 stage D CRCs from this study and 42 stage A and 62 stage D CRCs from expO. For the expO dataset, separate comparisons were performed for primary stage D cancers and distant metastases to identify gene expression maintained during metastatic spread. For each cohort, MAS5.0-calculated signal intensities were normalized using the quantile normalization procedure implemented in robust multiarray analysis (RMA) (17 , 18 (link)) and the normalized data were log transformed (base 2). Probe sets which were not expressed or probe sets which showed a low variability across samples were excluded. Expression values were required to be above the median of all expression measurements in at least 25% of samples, and the interquartile range across the samples on the log scale was required to be at least 0.5. Genes mapping to sex chromosomes were excluded as cases were not matched by gender. A total of 6716 gene probes passed these filtering steps in all three sample sets.
Differentially expressed genes were identified using Significance Analysis of Microarrays (SAM) with a Wilcoxon rank-sum test and a false discovery rate (FDR) of 10% (19 (link)). Separate lists were generated for genes significantly up- or down-regulated in stage A CRCs as compared to stage D CRCs for each of the three comparisons. For differentially expressed genes identified repeatedly between cohorts, consistency of up- or down-regulation was assessed using Pearson’s chi-squared test.
Jorissen R.N., Gibbs P., Christie M., Prakash S., Lipton L., Desai J., Kerr D., Aaltonen L.A., Arango D., Kruhøffer M., Ørntoft T.F., Andersen C.L., Gruidl M., Kamath V.P., Eschrich S., Yeatman T.J, & Sieber O.M. (2009). Metastasis-associated gene expression changes predict poor outcomes in patients with Dukes’ stage B and C colorectal cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, 15(24), 7642-7651.
Publication 2009
Calcibiotic Root Canal Sealer Down-Regulation Gene Expression Genes Genes, vif Microarray Analysis Neoplasm Metastasis Staging, Cancer Strains
2
Comprehensive CRC Cohort for Molecular Profiling
Fresh-frozen tumor specimens from 293 consecutive CRC patients were retrieved from the tissue banks of the Royal Melbourne Hospital, Western Hospital and Peter MacCallum Cancer Center in Australia, and the H. Lee Moffitt Cancer Center in the United States; individuals who had received preoperative chemo- and/or radiotherapy or for whom tumor-derived total RNA was inadequate for microarray analysis (RIN < 6) were excluded. All patients gave informed consent, and this study was approved by the medical ethics committees of all sites. Patient median age at diagnosis was 67 years (range 26 to 92 years). All specimens were derived from primary carcinomas and were snap-frozen in liquid nitrogen immediately after surgery for storage at −80°C. Cases comprised 44 stage A, 95 stage B, 93 stage C and 61 stage D cancers; 252 were localized to the colon and 40 to the rectum, with one case missing this information. 22 of 94 patients who had stage B disease and 64 of 91 patients who had stage C disease had received standard adjuvant chemotherapy (either single agent 5-fluouracil/capecitabine or 5-fluouracil and oxaliplatin) or postoperative concurrent chemoradiotherapy (50.4 Gy in 28 fractions with concurrent 5-fluorouracil) according to hospital protocols. All patients were assessed annually. For stage B and C patients, follow-up and additional clinical data including patient gender and TNM staging were collected by Biogrid Australia 1 for Australian patients and the Moffitt Cancer Center Tumor Registry for US patients. The median duration of follow-up was 47.8 months (range 0.9 to 118.6 months) for the 140 patients without recurrence, and 19.1 months (range 1.6 to 93.7 months) for the 48 patients with local or distant recurrence. The median follow-up for all 188 patients was 37.2 months (range 0.9 to 118.6 months).
Total RNA was extracted using Trizol reagent (Invitrogen) from CRC samples containing >60% tumor cells. All samples included showed good integrity of 18S and 28S ribosomal bands (RIN > 6) using a 2100 Bioanalyzer (Agilent Technologies). Total RNA was labeled and hybridized to HG-U133Plus2.0 GeneChip arrays (Affymetrix) according to the manufacturer’s instructions. The microarray data on a subset of 174 tumors have been published previously (NCBI Gene Expression Omnibus, GSE5206 and GSE13067).
In addition, published gene expression data were retrieved for 42 stage A CRCs, 83 stage B, 73 stage C and 62 stage D CRCs analyzed as part of the Expression Project for Oncology (expO) 2 using HG-U133Plus2.0 GeneChip arrays (Affymetrix) (Supplementary Table S1). Of the 62 stage D CRCs, 32 were primary cancer and 30 were metastectomy specimens. None of the primary cancer patients had received preoperative therapy, but 17 metastectomy specimens were from patients who had received adjuvant chemotherapy treatment prior to resection. Data processing and analysis were performed using the statistical software package R (15 ) and appropriate Bioconductor packages (16 (link)).
Jorissen R.N., Gibbs P., Christie M., Prakash S., Lipton L., Desai J., Kerr D., Aaltonen L.A., Arango D., Kruhøffer M., Ørntoft T.F., Andersen C.L., Gruidl M., Kamath V.P., Eschrich S., Yeatman T.J, & Sieber O.M. (2009). Metastasis-associated gene expression changes predict poor outcomes in patients with Dukes’ stage B and C colorectal cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, 15(24), 7642-7651.
Publication 2009
Calcibiotic Root Canal Sealer Capecitabine Carcinoma Cells Chemotherapy, Adjuvant Colon Concurrent Chemoradiotherapy Diagnosis Ethics Committees Fluorouracil Freezing Gender Gene Chips Gene Expression Malignant Neoplasms Microarray Analysis Neoadjuvant Therapy Neoplasms Nitrogen Operative Surgical Procedures Oxaliplatin Patients Pharmaceutical Adjuvants Pharmacotherapy Radiotherapy Rectum Recurrence Ribosomes RNA, Neoplasm trizol
3
Correlating TGF-beta and TBRS Expression in CRC

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Publication 2012
Adenoma Calcibiotic Root Canal Sealer Cancer of Colon Carcinoma Colon Disease Progression Homo sapiens Hospital Administration Malignant Neoplasms Neoplasms Patients RNA, Messenger TGFB1 protein, human TGFB2 protein, human TGFB3 protein, human Transforming Growth Factor beta
4
Molecular Profiling of Colorectal Cancers

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Publication 2014
Calcibiotic Root Canal Sealer CpG Islands Diploid Cell Homo sapiens Mutation Phenotype PIK3CA protein, human TP53 protein, human
5
Variant Calling and Mutation Profiling
The processing of exome-sequencing data from1 (link)
and TCGA2 (link) involved variant calling on matched-normal
pairs using Mutect3 . A mutation was considered if the
depth of coverage was ≥10 and at least 3 reads supported the variant. Mutations that
aligned to a more than one genomic location were discarded. The WGS gastric cancers4 (link) were processed using VarScan25 (link), with minimum depth of coverage for a mutation being 10x and at least 3
reads supporting the variant. Non-CRCs in the TCGA had mutations called using Mutect according
to the pipeline described in ref6 (link). Microsatellite
instability in the TCGA colon cancer samples was called using MSIsensor7 (link). Annotation was performed with ANNOVAR8 (link).
To fit the neutral model to allele frequency data we considered only variants with
allele frequency in the range [fmax,fmin] corresponding
to [t0,t] in equation [2]. The low boundary fmin reflects the
limit for the reliable detectability of low-frequency mutations in NGS data, which is in the
order of 10%3 . The high boundary
fmax is necessary to filter out public mutations that were present
in the first transformed cell. In the case of diploid tumors, clonal mutations are expected at
fmax=0.5 (mutations with 50% allelic frequency are heterozygous
public or clonal), in the case of triploid tumors, this threshold drops to 0.33 and in the case
of tetraploid neoplasms, it drops to 0.25. For all samples we used a boundary of [0.12-0.24] to
account only for reliably called subclonal mutations and tumor purity in the samples. All the
samples considered in this study were reported to have tumor purity ≥70% and a minimum
of 12 reliably called private mutations within the fit boundary. Once these conditions were met
in a sample, equation [7] was used to perform
the fit as illustrated in Figure 1B and 2B. In particular, for x=1/f, equation [7] becomes a linear model with slope
μ/β and intercept –μ/(β
fmax). We exploited the intercept constraint to perform a more
restrictive fit using the model
y=m(x-1/fmax)+0.
Copy-number changes (allelic deletion or duplication) can alter the frequency of a
variant in a manner that is not described by equation
[7]. We assessed the impact of copy-number alterations (CNAs) on our estimates of the
mutation rate within the TCGA colorectal cancer samples by using the paired publically
available segmented SNP-array data to exclude somatic mutations that fell within regions of
CNA. CNAs were identified having an absolute log-R-ratio>0.5, and the model fitting was
performed only on diploid regions of the genome. In the gastric cancer cohort, regions with
copy number changes were identified using Sequenza9 (link) and
removed from the analysis. Mutation rates were adjusted to the size of the resulting diploid
genome. Supplementary Figures 2 and
5 demonstrate the robustness of our
analysis to copy number changes. R2 values were independent from
the mean coverage of mutations (p=0.32), the total number of mutations in the
sample (p=0.40), the mutation rate (p=0.11), or the number of
mutations within the model range (p=0.65).
Williams M.J., Werner B., Barnes C.P., Graham T.A, & Sottoriva A. (2016). Identification of neutral tumor evolution across cancer types. Nature genetics, 48(3), 238-244.
Publication 2016
Alleles Calcibiotic Root Canal Sealer Cancer of Colon Clone Cells Colorectal Carcinoma Copy Number Polymorphism Deletion Mutation Diploid Cell Diploidy Gastric Cancer Genome Germ Cells Metin Mutation Neoplasms Stomach Tetraploidy Triploidy

Most recents protocols related to «Calcibiotic Root Canal Sealer»

1
Subcutaneous Tumor Inoculation in Mice
Female BALB/C mice (6–8 weeks) were purchased from Changsheng biotechnology, and they were fed in an SPF (specific pathogen–free) animal facility. CRCs and fibroblasts were separately suspended at 2 × 106/ml in DMEM-containing antibiotics and inoculated subcutaneously into the back of these mice that were maintained in the SPF environment (0.1 ml per site/animal). The animal study was reviewed and approved by Animal Care and Use Committee of the Northeastern University Committee, China.
Zhang Q., Wang C., Li R., Liu J., Wang J., Wang T, & Wang B. (2023). The BAP31/miR-181a-5p/RECK axis promotes angiogenesis in colorectal cancer via fibroblast activation. Frontiers in Oncology, 13, 1056903.
Full text: Click here
Publication 2023
Animals Antibiotics, Antitubercular Calcibiotic Root Canal Sealer Females Fibroblasts Mice, House Mice, Inbred BALB C Specific Pathogen Free
2
Establishing and Characterizing BAP31-Modified Colorectal Cancer Cells
Human umbilical vein endothelial cells (HUVECs), human normal lung fibroblast cells (WI-38), human CRCs (HCT116 and DLD-1), mouse embryonic fibroblasts (NIH/3T3), and mouse CRCs (MC38) were cultured in the Dulbecco’s modified Eagle’s medium (DMEM), supplementing with 10% fetal bovine serum, streptomycin (100 U/ml), and penicillin (100 U/ml). They were cultured in a humidified atmosphere of 5% CO2 at 37°C.
BAP31-overexpressing CRCs and BAP31-knockdown CRCs were established as previously (18 (link)). All of the constructed plasmids were verified by sequencing. Real-time Quantitative Polymerase Chain Reaction (qPCR) and Western blotting analysis were used to detect gene expressions.
Zhang Q., Wang C., Li R., Liu J., Wang J., Wang T, & Wang B. (2023). The BAP31/miR-181a-5p/RECK axis promotes angiogenesis in colorectal cancer via fibroblast activation. Frontiers in Oncology, 13, 1056903.
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Publication 2023
Atmosphere BCAP31 protein, human Calcibiotic Root Canal Sealer Cells Culture Media Eagle Embryo Fetal Bovine Serum Fibroblasts Gene Expression Homo sapiens Human Umbilical Vein Endothelial Cells Lung Mus NIH 3T3 Cells Penicillins Plasmids Real-Time Polymerase Chain Reaction Streptomycin Western Blot
3
Investigating ACOX1 in Colorectal Cancer
Forty-five early CRC samples and 51 normal adjacent tissues were used to analyze ACOX1 transcript levels, and 24 pairs of these samples were used to analyze ACOX1, DUSP14, and β-catenin protein levels. Fifteen fresh CRC samples and matched normal adjacent tissues were used to analyze PA levels. 192 CRC samples were made into TMA to analyze indicated protein levels and overall survival. All samples were obtained from the Sixth Affiliated Hospital of Sun Yat-sen University. The diagnosis of CRCs was verified by histological review. Our study was approved by the Ethics Committee of the Sixth Affiliated Hospital of Sun Yat-sen University (2020ZSLYEC-232). All patients signed written informed consent forms before treatment.
Zhang Q., Yang X., Wu J., Ye S., Gong J., Cheng W.M., Luo Z., Yu J., Liu Y., Zeng W., Liu C., Xiong Z., Chen Y., He Z, & Lan P. (2023). Reprogramming of palmitic acid induced by dephosphorylation of ACOX1 promotes β-catenin palmitoylation to drive colorectal cancer progression. Cell Discovery, 9, 26.
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Publication 2023
Calcibiotic Root Canal Sealer Catenins Diagnosis Ethics Committees, Clinical Patients Proteins Tissues
4
Colonoscopy Surveillance in Lynch Syndrome
A single-center, observational cohort study was conducted at Karolinska University Hospital in Stockholm, Sweden. The study considered LS patients with an MMR gene mutation who were followed at the Karolinska University Hospital from 1989 to April 2021. All MMR gene mutations were confirmed according to the InSight Variant Committee’s classification (20 (link)) or reported to be pathogenic by the hospital’s genetics department if the variant was unknown. Of 427 LS patients registered at the clinic, 366 were eligible for inclusion. Part of the cohort has previously been described (18 (link)).
After the MMR gene mutation had been confirmed, patients were recommended an index colonoscopy within 3 months. If the colonoscopy was “clean”, surveillance continued with a recommended interval of 1-2 years.
CRCs were classified as detected before surveillance if they had been detected before the MMR gene mutation was confirmed. A CRC detected at index or after index (where index is defined as the first colonoscopy after LS diagnosis is given, and after index is defined as the second colonoscopy after the MMR gene mutation is confirmed) was classified as detected during surveillance. Patients with multiple CRCs, detected both before and during surveillance, are also included in the “during surveillance” group below. Colonoscopies were counted and analyzed up until CRC detection. To study interval cancers only, the colonoscopies detecting CRC had to follow a “clean” examination within a reasonable timeframe. Accordingly, index CRCs were excluded from the TNM distribution and surveillance interval calculations. Underweight, normal weight, overweight and obese were defined as BMI (<18.5 kg/m2), (18.5–24.9 kg/m2), (18.5-<25.0 kg/m2) and (25.0-<30.0 kg/m2), respectively.
Jamizadeh N., Walton Bernstedt S., Haxhijaj A., Andreasson A., Björk J., Forsberg A, & Backman A.S. (2023). Endoscopic surveillance of Lynch syndrome at a highly specialized center in Sweden: An observational study of interval colorectal cancer and individual risk factors. Frontiers in Oncology, 13, 1127707.
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Publication 2023
Calcibiotic Root Canal Sealer Colonoscopy Diagnosis Genes Malignant Neoplasms Mutation Obesity pathogenesis Patients
5
Older Adult Interventional Trials
Participants were PIs (N = 20) and CRCs (N = 20). Participants from each group were identified using publicly available information and snowball recruitment. PIs and CRCs were identified via ClinicalTrials.gov using advanced search criteria to ensure they all conducted interventional trials with older adults [60 ].
Mozersky J., Solomon E.D., Baldwin K., Wroblewski M., Parsons M., Goodman M, & DuBois J.M. (2023). Barriers to Using Legally Authorized Representatives in Clinical Research with Older Adults. Journal of Alzheimer's Disease Reports, 7(1), 135-149.
Publication 2023
Aged Calcibiotic Root Canal Sealer

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Trizol reagent by Thermo Fisher Scientific
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More about "Calcibiotic Root Canal Sealer"

Calcibiotic root canal sealers are a specialized class of dental materials used to fill and seal the internal chamber (root canal) of a tooth after the soft pulp tissue has been removed.
These bioceramic-based sealers are designed to promote the healing and regeneration of the surrounding bone and tissues, while also providing a secure seal to prevent bacterial infection.
Key features of calcibiotic root canal sealers include their antimicrobial properties and ability to stimulate new bone formation - critical for ensuring long-term tooth health and function following endodontic (root canal) procedures.
Researchers can leverage PubCompare.ai, an AI-driven protocol optimization platform, to streamline their evaluations of different calcibiotic root canal sealer formulations and protocols.
By locating the best protocols from literature, preprints, and patents, and performing data-driven comparisons, scientists can identify the optimal products and procedures for their research needs.
This can help accelerate discoveries in this important area of dental science.
Beyond calcibiotic root canal sealers, researchers may also find value in other tools and reagents such as TRIzol for RNA extraction, GraphPad Prism 5 for data analysis, the HiSeq 2000 sequencing platform, the EZ DNA Methylation Kit for epigenetic studies, and the StepOnePlus Real-Time PCR System for gene expression analysis.
By incorporating a diverse set of techniques and technologies, scientists can unlock new insights and advance their understanding of dental materials, tissue regeneration, and endodontic therapies.