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      Evidence of sex differences in cancer‐related cardiac complications in mouse models of pancreatic and liver cancer

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          Abstract

          Abnormal heart rate variability (HRV) is commonly observed in cancer patients who have undergone targeted therapy and/or surgery, yet the effects of cancer itself on cardiac function remain underexplored. Specifically, there is limited knowledge about sex‐specific manifestations of HRV in cancer patients. Transgenic mouse models are widely used to study different types of cancer. Here, we aimed to investigate the sex‐specific effects of cancer on cardiac function using transgenic mouse models of pancreatic and liver cancers. This study used male and female transgenic mice with cancer and wild‐type controls. Cardiac function was assessed by recording electrocardiograms in conscious mice. RR intervals were detected to determine HRV using time and frequency domain analyses. Histological analysis with Masson's trichrome staining was performed to determine structural changes. In females, increased HRV was observed in both pancreatic and liver cancer‐bearing mice. In contrast, in males, increased HRV was observed only in the liver cancer group. Male pancreatic cancer mice demonstrated autonomic balance shift showing an increase in parasympathetic to sympathetic tone. The heart rate (HR) was higher in control and liver cancer male mice groups than in females. Histological analysis did not show significant sex differences but suggested a higher degree of remodeling in liver cancer mice than in control, specifically in the right atrium and left ventricle. This study revealed sex differences in cancer's HR modulation. Specifically, female cancer mice had lower median HR and higher HRV. These findings indicate that sex must be considered when using HRV as a cancer biomarker.

          Abstract

          Female mice developed higher heart rate variability (HRV) and lower heart rate in the liver and pancreatic cancer groups than control mice. The male pancreatic cancer group showed an autonomic balance shift toward increased parasympathetic tone. The male liver cancer group demonstrated increased HRV.

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          An Overview of Heart Rate Variability Metrics and Norms

          Healthy biological systems exhibit complex patterns of variability that can be described by mathematical chaos. Heart rate variability (HRV) consists of changes in the time intervals between consecutive heartbeats called interbeat intervals (IBIs). A healthy heart is not a metronome. The oscillations of a healthy heart are complex and constantly changing, which allow the cardiovascular system to rapidly adjust to sudden physical and psychological challenges to homeostasis. This article briefly reviews current perspectives on the mechanisms that generate 24 h, short-term (~5 min), and ultra-short-term (<5 min) HRV, the importance of HRV, and its implications for health and performance. The authors provide an overview of widely-used HRV time-domain, frequency-domain, and non-linear metrics. Time-domain indices quantify the amount of HRV observed during monitoring periods that may range from ~2 min to 24 h. Frequency-domain values calculate the absolute or relative amount of signal energy within component bands. Non-linear measurements quantify the unpredictability and complexity of a series of IBIs. The authors survey published normative values for clinical, healthy, and optimal performance populations. They stress the importance of measurement context, including recording period length, subject age, and sex, on baseline HRV values. They caution that 24 h, short-term, and ultra-short-term normative values are not interchangeable. They encourage professionals to supplement published norms with findings from their own specialized populations. Finally, the authors provide an overview of HRV assessment strategies for clinical and optimal performance interventions.
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            Role of oncogenic KRAS in the diagnosis, prognosis and treatment of pancreatic cancer

            Pancreatic ductal adenocarcinoma (PDAC) is predicted to be the second most common cause of death within the next 10 years. The prognosis for this disease is poor despite diagnostic progress and new chemotherapeutic regimens. The oncogenic KRAS mutation is the major event in pancreatic cancer; it confers permanent activation of the KRAS protein, which acts as a molecular switch to activate various intracellular signalling pathways and transcription factors inducing cell proliferation, migration, transformation and survival. Several laboratory methods have been developed to detect KRAS mutations in biological samples, including digital droplet PCR (which displays high sensitivity). Clinical studies have revealed that a KRAS mutation assay in fine-needle aspiration material combined with cytopathology increases the sensitivity, accuracy and negative predictive value of cytopathology for a positive diagnosis of pancreatic cancer. In addition, the presence of KRAS mutations in serum and plasma (liquid biopsies) correlates with a worse prognosis. The presence of mutated KRAS can also have therapeutic implications, whether at the gene level per se, during its post-translational maturation, interaction with nucleotides and after activation of the various oncogenic signals. Further pharmacokinetic and toxicological studies on new molecules are required, especially small synthetic molecules, before they can be used in the therapeutic arsenal for pancreatic ductal adenocarcinoma.
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              Myocardial infarction accelerates breast cancer via innate immune reprogramming

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                Author and article information

                Contributors
                irefimov@gmail.com
                Journal
                Physiol Rep
                Physiol Rep
                10.1002/(ISSN)2051-817X
                PHY2
                physreports
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                2051-817X
                26 April 2023
                April 2023
                : 11
                : 8 ( doiID: 10.1002/phy2.v11.8 )
                : e15672
                Affiliations
                [ 1 ] Department of Biomedical Engineering The George Washington University Washington District of Columbia USA
                [ 2 ] The George Washington Cancer Center The George Washington University School of Medicine and Health Sciences Washington District of Columbia USA
                [ 3 ] Department of Biomedical Engineering Northwestern University Chicago Illinois USA
                [ 4 ] Department of Anatomy and Cell Biology The George Washington University School of Medicine and Health Sciences Washington District of Columbia USA
                [ 5 ] Department of Medicine Northwestern University Chicago Illinois USA
                Author notes
                [*] [* ] Correspondence

                Igor R. Efimov, Department of Biomedical Engineering, Northwestern University, Chicago, IL, USA.

                Email: irefimov@ 123456gmail.com

                Author information
                https://orcid.org/0000-0002-1483-5039
                Article
                PHY215672 PHY2-2022-09-0395.R1
                10.14814/phy2.15672
                10133859
                37102225
                b8bdfeb1-8d82-453f-9b25-759c5d8758ee
                © 2023 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 March 2023
                : 23 September 2022
                : 29 March 2023
                Page count
                Figures: 5, Tables: 0, Pages: 9, Words: 5794
                Funding
                Funded by: Fondation Leducq , doi 10.13039/501100001674;
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                April 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.7 mode:remove_FC converted:27.04.2023

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