Browsing by Author "Dubois, Karen"
Now showing 1 - 3 of 3
Results Per Page
Sort Options
Publication Hypoglycemia and glycemic variability of people with type 1 diabetes with lower and higher physical activity loads in free-living conditions using continuous subcutaneous insulin infusion with predictive low-glucose suspend system(2023) Montt, Denise; Sánchez, Raimundo; Dubois, Karen; Leppe, Jaime; Onetto, MaríaIntroduction: Maintaining glycemic control during and after physical activity (PA) is a major challenge in type 1 diabetes (T1D). This study compared the glycemic variability and exercise-related diabetic management strategies of adults with T1D achieving higher and lower PA loads in nighttime-daytime and active- sedentary behavior hours in free-living conditions. Research design and methods: Active adults (n=28) with T1D (ages: 35±10 years; diabetes duration: 21±11 years; body mass index: 24.8±3.4 kg/m2; glycated hemoglobin A1c: 6.9±0.6%) on continuous subcutaneous insulin delivery system with predictive low glucose suspend system and glucose monitoring, performed different types, duration and intensity of PA under free-living conditions, tracked by accelerometer over 14 days. Participants were equally divided into lower load (LL) and higher load (HL) by median of daily counts per minute (61122). Glycemic variability was studied monitoring predefined time in glycemic ranges (time in range (TIR), time above range (TAR) and time below range (TBR)), coefficient of variation (CV) and mean amplitude of glycemic excursions (MAGE). Parameters were studied in defined hours timeframes (nighttime-daytime and active-sedentary behavior). Self-reported diabetes management strategies were analysed during and post-PA. Results: Higher glycemic variability (CV) was observed in sedentary hours compared with active hours in the LL group (p≤0.05). HL group showed an increment in glycemic variability (MAGE) during nighttime versus daytime (p≤0.05). There were no differences in TIR and TAR across all timeframes between HL and LL groups. The HL group had significantly more TBR during night hours than the LL group (p≤0.05). Both groups showed TBR above recommended values. All participants used fewer post-PA management strategies than during PA (p≤0.05). Conclusion: Active people with T1D are able to maintain glycemic variability, TIR and TAR within recommended values regardless of PA loads. However, the high prevalence of TBR and the less use of post-PA management strategies highlights the potential need to increase awareness on actions to avoid glycemic excursions and hypoglycemia after exercise completion.Publication Pannexin-1 expression in tumor cells correlates with colon cancer progression and survival(2024) Fierro, Aaron; Landskron, Glauben; Camhi, Ilan; Basterrechea, Benjamín; Parada, Daniela; Lobos-González, Lorena; Dubois, Karen; Araneda, Catalina; Romero, Camila; Domínguez, Antonia; Vásquez, Gonzalo; López, Francisco; Alvarez, Karin; González, Carlos; Hager, Carolina; Balboa, Elisa; Eugenin, Eliseo; Hermoso, Marcela; De la Fuente, MarjorieAims: Pannexin-1 (PANX1) is a hemichannel that releases ATP upon opening, initiating inflammation, cell proliferation, and migration. However, the role of PANX1 channels in colon cancer remains poorly understood, thus constituting the focus of this study. Main methods: PANX1 mRNA expression was analyzed using multiple cancer databases. PANX1 protein expression and distribution were evaluated by immunohistochemistry on primary tumor tissue and non-tumor colonic mucosa from colon cancer patients. PANX1 inhibitors (probenecid or 10Panx) were used to assess colon cancer cell lines viability. To study the role of PANX1 in vivo, a subcutaneous xenograft model using HCT116 cells was performed in BALB/c NOD/SCID immunodeficient mice to evaluate tumor growth under PANX1 inhibition using probenecid. Key findings: PANX1 mRNA was upregulated in colon cancer tissue compared to non-tumor colonic mucosa. Elevated PANX1 mRNA expression in tumors correlated with worse disease-free survival. PANX1 protein abundance was increased on tumor cells compared to epithelial cells in paired samples, in a cancer stage-dependent manner. In vitro and in vivo experiments indicated that blocking PANX1 reduced cell viability and tumor growth. Significance: PANX1 can be used as a biomarker of colon cancer progression and blocking PANX1 channel opening could be used as a potential therapeutic strategy against this disease.Item Variants in DNA double-strand break repair genes and risk of familial breast cancer in a South American population(2010) Jara, Lilian; Dubois, Karen; Gaete, Daniel; de Mayo, Tomas; Ratkevicius, Nikalai; Bravo, Teresa; Margarit, Sonia; Blanco, Rafael; Gomez, Fernando; Waugh, Enrique; Peralta, Octavio; Reyes, Jose M.; Ibanez, Gladys; Gonzalez-Hormazabal, PatricioThe double-strand break (DSB) DNA repair pathway has been implicated in breast cancer (BC). RAD51 and its paralogs XRCC3 and RAD51D play an important role in the repair of DSB through homologous recombination (HR). Some polymorphisms including XRCC3-Thr241Met, RAD51-135G[C, and RAD51D-E233G have been found to confer increased BC susceptibility. In order to detect novel mutations that may contribute to BC susceptibility, 150 patients belonging to 150 Chilean BRCA1/2-negative families were screened for mutations in XRCC3. No mutations were detected in the XRCC3 gene. In addition, using a case–control design we studied the XRCC3-Thr241Met, and RAD51D-E233G polymorphisms in 267 BC cases and 500 controls to evaluate their possible association with BC susceptibility. The XRCC3 Met/Met genotype was associated with an increased BC risk (P = 0.003, OR = 2.44 [95%CI 1.34–4.43]). We did not find an association between E233G polymorphism and BC risk. We also analyzed the effect of combined genotypes among RAD51-135G[C, Thr241Met, and E233G polymorphisms on BC risk. No interaction was observed between Thr241Met and 135G[C. The combined genotype Thr/Met–E/G was associated with an increased BC risk among women who (a) have a family history of BC, (b) are BRCA1/2-negative, and (c) were \50 years at onset (n = 195) (P = 0.037, OR = 10.5 [95%CI 1.16–94.5]). Our results suggested that the variability of the DNA HR repair genes XRCC3 and RAD51D may play a role in BC risk, but this role may be underlined by a mutual interaction between these genes. These findings should be confirmed in other populations.