Citations

Abstract Viral infections are estimated to contribute to 12% to 20% of all cancers worldwide, with virus-driven malignancies disproportionately affecting low- and middle-income countries, whereas metabolic and nonviral factors predominate in high-income regions. Key oncogenic viruses that cause solid tumors include high-risk human papillomaviruses, Epstein–Barr virus, hepatitis B virus, hepatitis C virus, Kaposi sarcoma–associated herpesvirus, and Merkel cell polyomavirus. Immune checkpoint inhibitors (ICI) have revolutionized cancer therapy by boosting immune responses against tumors. Although viral infection–associated tumors often exhibit “hot” immune profiles, clinical outcomes with ICIs remain inconsistent. Some studies report improved survival in virus-associated cancers, whereas others indicate no clear benefit, which might reflect high variability in tumor microenvironments and immune responses. In this review, we aim to explore the direct and indirect contribution of different viruses to carcinogenesis in solid tumors, with a particular focus on immunotherapy effectiveness based on infection status.

Abstract Despite much of the past 2 years being engulfed by the devastating consequences of the SAR‐CoV‐2 pandemic, significant progress, even breathtaking, occurred in the field of chronic myeloid malignancies. Some of this was show‐cased at the 15th Post‐American Society of Hematology (ASH) and the 25th John Goldman workshops on myeloproliferative neoplasms (MPN) held on 9th‐10th December 2020 and 7th‐10th October 2021, respectively. The inaugural Post‐ASH MPN workshop was set out in 2006 by John Goldman (deceased) and Tariq Mughal to answer emerging translational hematology and therapeutics of patients with these malignancies. Rather than present a resume of the discussions, this perspective focuses on some of the pivotal translational hematology and therapeutic insights in these diseases.

Magnetic resonance elastography (MRE) is a phase contrast–based MRI technique that can measure displacement due to propagating mechanical waves, from which material properties such as shear modulus can be calculated. Magnetic resonance elastography can be thought of as quantitative, noninvasive palpation. It is increasing in clinical importance, has become widespread in the diagnosis and staging of liver fibrosis, and additional clinical applications are being explored. However, publications have reported MRE results using many different parameters, acquisition techniques, processing methods, and varied nomenclature. The diversity of terminology can lead to confusion (particularly among clinicians) about the meaning of and interpretation of MRE results. This paper was written by the MRE Guidelines Committee, a group formalized at the first meeting of the ISMRM MRE Study Group, to clarify and move toward standardization of MRE nomenclature. The purpose of this paper is to (1) explain MRE terminology and concepts to those not familiar with them, (2) define “good practices” for practitioners of MRE, and (3) identify opportunities to standardize terminology, to avoid confusion.

AbstractHeart failure (HF) patients appear to exhibit impaired thermoregulatory capacity during passive heating, as evidenced by diminished vascular conductance. Although some preliminary studies have described the thermoregulatory response to passive heating inHF, responses during exercise in the heat remain to be described. Therefore, the aim of this study was to compare thermoregulatory responses inHFand controls (CON) during exercise in the heat. TenHF(NYHAclasses I–II) and eightCONwere included. Core temperature (Tc), skin temperature (Tsk), and cutaneous vascular conductance (CVC) were assessed at rest and during 1 h of exercise at 60% of maximal oxygen uptake. Metabolic heat production (Hprod) and the evaporative requirements for heat balance (Ereq) were also calculated. Whole‐body sweat rate was determined from pre–post nude body mass corrected for fluid intake. WhileHprod(HF: 3.9 ± 0.9;CON: 6.4 ± 1.5 W/kg) andEreq(HF: 3.3 ± 0.9;CON: 5.6 ± 1.4 W/kg) were lower (P < 0.01) forHFcompared toCON, both groups demonstrated a similar rise inTc(HF: 0.9 ± 0.4;CON: 1.0 ± 0.3°C). Despite this similar rise inTc,Tsk(HF: 1.6 ± 0.7;CON: 2.7 ± 1.2°C), and the elevation inCVC(HF: 1.4 ± 1.0;CON: 3.0 ± 1.2 au/mmHg) was lower (P < 0.05) inHFcompared toCON. Additionally, whole‐body sweat rate (HF: 0.36 ± 0.15;CON: 0.81 ± 0.39 L/h) was lower (P = 0.02) inHFcompared toCON. Patients withHFappear to be limited in their ability to manage a thermal load and distribute heat content to the body surface (i.e., skin), secondary to impaired circulation to the periphery.

Purpose In this study, the authors examined mean volumes of discrete sips performed by healthy adults from straws varying in internal diameter. Method Forty healthy adults sipped water from each of 7 straws varying in internal diameter (0.65–5.00 mm). Bolus volumes associated with 3 discrete sips were recorded under each sip condition. Results Straw diameter had a significant effect on bolus size, with the smallest diameter straws eliciting the smallest bolus volumes. Bolus volumes did not vary according to age or sex. Considerable intersubject variation was observed, particularly for the straws with the largest diameters. Intrasubject variability across 3 trials was minimal. Conclusions The findings support the hypothesis that narrower straw diameters are associated with smaller bolus volumes in healthy adults. Additional study is needed to determine whether individuals with dysphagia demonstrate similar patterns of bolus size associated with straws varying in internal diameter and whether such variations have clinical benefit.

Abstract— Coronary artery disease (CAD) is the leading cause of mortality in the developed world. Although several CAD risk factors, including measures of lipid metabolism, obesity, and blood pressure, have a genetic basis, many genes for CAD susceptibility have yet to be identified. Coronary atherosclerosis is the major cause of CAD, but many with coronary atherosclerosis lack symptoms. Thus, a major limitation of using symptomatic CAD endpoints (eg, sudden coronary death, myocardial infarction) as a study outcome is substantial disease misclassification. Coronary artery calcification (CAC) is part of the atherosclerotic process and is an independent predictor of CAD endpoints. In the present study, CAC was noninvasively quantified by electron beam computed tomography. We performed genome-wide multipoint mode-of-inheritance-free linkage analysis on affected sib pairs, defined as being ≥ the 70th sex- and age-specific percentile for CAC quantity, in a sample of 29 families enriched for hypertension. Almost 95% of participants were asymptomatic for CAD. Our LOD score (log 10 odds in favor of linkage) results provide evidence that chromosomal regions 6p21.3 (maximum LOD score=2.22, P =0.00070) and 10q21.3 (maximum LOD score=3.24, P =0.000057) may harbor genes associated with subclinical coronary atherosclerosis.