[Purpose] To verify the identification of the anaerobic threshold through the double product breakpoint (DPBP) method for individuals with type 2 diabetes. [Subjects and Methods] Nine individuals with T2D (7 females; age=63.2 ± 8.9 y) and 10 non-diabetic (ND) (7 females; age=58.3 ± 7.8 y) performed an incremental exercise test on a cycle ergometer. Heart rate (HR), blood pressure (BP) and expired gas were measured at the end of each stage. The ventilatory threshold (VT) and DPBP were considered as the exercise intensities above which an over proportional increases in VE and DP were observed in relation to increasing workload. [Results] No differences were observed between the workloads, HR and VO2 corresponding to the AT identified respectively by VT and DPBP. For the T2D, strong correlations between VT and DBPB workloads (r=0.853), HR (r=0.714), and VO2 (r=0.863) were found. These relationships were similar to those found for the control group (r=0.923; r=0.881; and r=0.863, respectively). [Conclusion] These results demonstrate that the DPBP enables for the prediction of AT and correlated well the VT in both the T2D and ND participants.
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http://dx.doi.org/10.1589/jpts.28.1775 | DOI Listing |
Am J Cancer Res
December 2024
Hangzhou DAC Biotechnology Co., Ltd. No. 369 Qiaoxin Road, Qiantang District, Hangzhou 310018, Zhejiang, China.
Gastric cancer is a common malignant tumor with high incidence and mortality. The overexpression of Human epidermal growth factor receptor 2 (HER2) is associated with increased metastatic potential and poor clinical outcome in gastric cancer. Despite the proven clinical response rates of approved HER2-targeted therapies, including Trastuzumab combined with chemotherapy, their limited long-term clinical benefits and inevitable disease progression still pose significant challenges to the clinical treatment of gastric cancer.
View Article and Find Full Text PDFGenetic medicines, including CRISPR/Cas technologies, extend tremendous promise for addressing unmet medical need in inherited retinal disorders and other indications; however, there remain challenges for the development of therapeutics. Herein, we evaluate genome editing by engineered Cas9 ribonucleoproteins (eRNP) in vivo via subretinal administration using mouse and pig animal models. Subretinal administration of adenine base editor and double strand break-inducing Cas9 nuclease eRNPs mediate genome editing in both species.
View Article and Find Full Text PDFG-quadruplexes (G4s) are four-stranded alternative secondary structures formed by guanine-rich nucleic acids and are prevalent across the human genome. G4s are enzymatically resolved using specialized helicases. Previous studies showed that DEAH-box Helicase 36 (DHX36/G4R1/RHAU), has the highest specificity and affinity for G4 structures.
View Article and Find Full Text PDFOphthalmol Sci
November 2024
Roche Pharmaceutical Research and Early Development, Translational Medicine Ophthalmology, Roche Innovation Center, Basel, Switzerland.
Objective: Nonproliferative diabetic retinopathy (NPDR) is a progressive disease that can lead to blindness. Current therapies for NPDR are invasive and not extensively used or accessible until the disease progresses, pointing to the need for an early noninvasive treatment. The objective of CANBERRA was to assess the safety, tolerability, and efficacy of oral administration of vicasinabin (RG7774) on the severity of diabetic retinopathy (DR) in participants with moderately severe to severe NPDR and good vision.
View Article and Find Full Text PDFToxicol Res
January 2025
Department of Pharmacology, College of Medicine, Chungnam National University, 266, Munhwa-ro, Jung-gu, Daejeon, 35015 Republic of Korea.
Over the last decade, the functions of PHD finger protein 20 (PHF20) in several signaling processes have been studied, including those of protein kinase B (PKB)-mediated phosphorylation, p53 regulation, muscle differentiation, and histone modification including histone H3 lysine 4 (H3K4) methylation. One PHF20 human mutation lacks the first nonspecific lethal complex of the component that binds to H3K4me2 to facilitate cancer cell survival. In carcinoma cells, PHF20 expression is regulated by PKB; PHF20 becomes phosphorylated when DNA is damaged, thus inhibiting the p53 activity that maintains cancer cell survival.
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