https://nova.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:53018 Wed 28 Feb 2024 16:09:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:53591 Wed 28 Feb 2024 16:00:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:53356 Wed 28 Feb 2024 15:24:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54997 Wed 27 Mar 2024 16:38:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45244 Wed 26 Oct 2022 15:43:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:25448 Wed 24 Nov 2021 15:53:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:25751 Wed 17 Nov 2021 16:31:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:30103 in vitro including conventional hemocytometer counting chamber, a luminescence-based assay that utilizes the change in the metabolic activity of viable cells as a measure of the relative number of cells, and a multi-mode cell imager that measures cell number using a counting algorithm. Each method presents its own advantages and disadvantages for the measurement of cell proliferation, including time, cost and high-throughput compatibility. This protocol demonstrates that each method could accurately measure cell proliferation over time, and was sensitive to detect growth at differing cellular densities. Additionally, measurement of cell proliferation using a cell imager was able to provide further information such as morphology, confluence and allowed for a continual monitoring of cell proliferation over time. In conclusion, each method is capable of measuring cell proliferation, but the chosen method is user-dependent.]]> Wed 17 Nov 2021 16:31:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54801 Wed 13 Mar 2024 11:41:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40650 Wed 13 Mar 2024 08:56:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:20669 Wed 11 Apr 2018 15:57:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14356 Wed 11 Apr 2018 15:41:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:14811 Wed 11 Apr 2018 14:25:00 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:13895 Wed 11 Apr 2018 11:47:28 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:22750 Wed 11 Apr 2018 10:56:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:23916 Wed 11 Apr 2018 10:32:03 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5046 Wed 11 Apr 2018 10:25:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:33387 34-weeks gestation; n=8) and gestational age matched preterm (31.6-35.1 weeks; n=8) and term normotensive controls were also compared. Agilent Human miRNA microarray v19 was used to detect up to 2006 miRNAs in four placentae from each group. Statistically different levels of expression were determined and refined using predictive modelling. Placental miRNAs predicted to target RAS mRNAs were identified in three databases. Differences detected on the array were confirmed for some miRNAs by semi-quantitative RT-PCR (qPCR, n=7-8 for all groups). Two differentially expressed miRNAs that were known to target human renal REN mRNA (miR-181a-5p and miR-663) were transfected into human HTR-8/SVneo trophoblast cells to examine their effect on placental REN expression and prorenin levels. In early gestation placentae, 186 miRNAs were differentially expressed compared with term placentae (109 increased, 77 decreased). Thirty of the differentially expressed miRNAs were predicted to target RAS components. In mid-gestation placentae, 117 miRNAs were differentially expressed compared with term placentae (69 increased, 48 decreased). Of these, 19 had RAS mRNAs as predicted targets. Eight miRNAs that were lower in early gestation and predicted to target RAS mRNAs were confirmed by qPCR. All showed an increase during gestation and could influence the transgestational profile of the human placental RAS. Additionally, on the array, three miRNAs predicted to target RAS mRNAs (miR-892c-3p, miR-378c and miR-514b-3p) were overexpressed in placentae from women with late-onset PE (P = 3.6E-10, P = 1.8E-05, P = 5.3E-06; respectively). miR-663, which suppresses renal REN mRNA expression, was overexpressed in early-onset PE placentae as determined by qRT-PCR analysis (P = 0.014). Transfection of miR-181a-5p and miR-663 into HTR-8/SVneo trophoblast cells suppressed REN mRNA expression (p = 0.05) and prorenin protein production (P = 0.001). Data can be found via GEO accession number GSE109832. Further validation that the differentially expressed miRNAs do indeed directly target RAS mRNAs and affect placental development and function is required. This study is limited by the small sample size. Therefore independent validation in a larger cohort is required.]]> Wed 02 Mar 2022 14:28:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:43522 10) (OR = 2.83, 95% CI: 0.94–8.11, p = 0.047), being overweight (≥25 kg/m2) (OR = 2.57, 95% CI: 1.04 – 6.38, p = 0.036), received fewer post-surgery rehabilitation treatment (OR = 2.37, 95% CI: 1.05–5.39, p = 0.036) and hypertension (OR = 2.38, 95% CI: 1.01–5.62, p = 0.043 ) were associated with an increased risk of BCRL. Meanwhile, multivariate analysis showed that multiple surgeries remained significant and elevated the likelihood of BCRL (OR = 5.83, 95% CI: 1.14–29.78, p = 0.034). Arm swelling was more prominent in the forearm area demonstrated by the highest difference of arm circumference measurement when compared to the upper arm ( 2.07 ± 2.48 vs. 1.34 ± 1.91 cm, p < 0.001). The total of skinfold thickness of the affected forearm was also significantly higher than the unaffected arms (p < 0.05) as evidenced by the ultrasound examination. The continuous search for risk factors in specific populations may facilitate the development of a standardized method to reduce the occurrence of BCRL and provide better management for breast cancer patients.]]> Tue 27 Jun 2023 09:47:57 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54539 Tue 27 Feb 2024 20:41:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:54475 Tue 27 Feb 2024 14:56:31 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:50644 Tue 01 Aug 2023 10:11:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:36559 Thu 28 Oct 2021 13:03:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:26531 Thu 28 Oct 2021 12:37:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:30240 EIG121) has been associated with breast and endometrial cancers, but its mechanism of action remains unknown. In a genome-wide search for tandem repeats, we found that EIG121 contains a short tandem repeat (STR) in its upstream regulatory region which has the potential to alter gene expression. The presence of this STR has not previously been analysed in relation to breast or endometrial cancer risk. Results: In this study, the lengths of this STR were determined by PCR, fragment analysis and sequencing using DNA from 223 breast cancer patients, 204 endometrial cancer patients and 220 healthy controls to determine if they were associated with the risk of developing breast or endometrial cancer. We found this repeat to be highly variable with the number of copies of the AG motif ranging from 27 to 72 and having a bimodal distribution. No statistically significant association was identified between the length of this STR and the risk of developing breast or endometrial cancer or age at diagnosis. Conclusions: The STR in the upstream regulatory region of EIG121 is highly polymorphic, but is not associated with the risk of developing breast or endometrial cancer in the cohorts analysed here. While this polymorphic STR in the regulatory region of EIG121 appears to have no impact on the risk of developing breast or endometrial cancer, its association with disease recurrence or overall survival remains to be determined.]]> Thu 28 Oct 2021 12:35:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40665 Thu 28 Jul 2022 12:15:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51863 Thu 21 Sep 2023 10:16:17 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41461 TP53 vary depending on the subtype, such that ER-negative tumours have a high rate, and in ER-positive tumours they are less common. Previous studies have implicated the intronic polymorphism in TP53 (rs17878362; or PIN3) with an increased risk of developing breast cancer, although little has been discerned on its prevalence in different subtypes. In this study, we investigated the prevalence of the PIN3 genotype in the blood of cohorts with ER-positive and the ER-negative subtype TNBC, and assessed its association with outcome. Methods: We genotyped 656 TNBC and 648 ER-positive breast cancer patients, along with 436 controls, and compared the prevalence of polymorphism rs17878362 in these cohorts. Results: We found there to be no differences in the prevalence of the PIN3 genotype between the ER-positive and TNBC cohorts. Furthermore, no statistically significant difference was observed in the outcome of patients in either cohort with respect to their PIN3 genotype. Conclusions: Taken together, our results do not support an association of the PIN3 genotype with increased breast cancer risk, either in ER-positive or ER-negative patients.]]> Thu 01 Sep 2022 11:19:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:6918 Sat 24 Mar 2018 08:34:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:13892 Sat 24 Mar 2018 08:19:33 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:12510 Sat 24 Mar 2018 08:18:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:18919 Sat 24 Mar 2018 07:59:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:19125 C) were found. In addition, five variants predicted to be protein-affecting were also identified. Our study shows that the prevalence of PALB2 germline mutations in individuals with TNBC is ~1%, similar to the prevalence of PALB2 germline mutation of 1% in familial non-BRCA1/2 breast cancer cohorts.]]> Sat 24 Mar 2018 07:55:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5683 Sat 24 Mar 2018 07:47:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:5341 Sat 24 Mar 2018 07:45:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:28878 Sat 24 Mar 2018 07:40:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:24332 Sat 24 Mar 2018 07:16:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40395 TP53 SNPs in exon 4 and intron 4 on cancer risk, clinicopathological features and expression of TP53 isoforms. The intron 4 SNPs were significantly over-represented in cohorts of mixed cancers compared to three ethnically matched controls, suggesting they confer increased cancer risk. Further analysis showed that heterozygosity at rs1042522(GC) and either of the two intronic SNPs rs9895829(TC) and rs2909430(AG) confer a 2.34-5.35-fold greater risk of developing cancer. These SNP combinations were found to be associated with shorter patient survival for glioblastoma and prostate cancer. Additionally, these SNPs were associated with tumor-promoting inflammation as evidenced by high levels of infiltrating immune cells and expression of the Δ133TP53 and TP53ß transcripts. We propose that these SNP combinations allow increased expression of the Δ133p53 isoforms to promote the recruitment of immune cells that create an immunosuppressive environment leading to cancer progression.]]> Mon 25 Jul 2022 09:15:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:42333 Mon 22 Aug 2022 11:06:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:20880 Mon 11 Mar 2019 12:15:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44184 Mon 10 Oct 2022 10:48:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:45818 Mon 07 Nov 2022 12:18:03 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:41279 Mon 01 Aug 2022 10:24:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:51723 Fri 15 Sep 2023 17:53:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:40033 Fri 15 Jul 2022 10:11:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:44474 Fri 14 Oct 2022 09:26:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/manager/Repository/uon:22586 Fri 10 Aug 2018 15:35:14 AEST ]]>