Browse Articles

Assessing climate change effects on Turkish tea farming through a dual approach using MMQR and machine learning

Abstract Climate change increasingly threatens the productivity of region-specific strategic agricultural products such as tea cultivation in Türkiye, posing a serious risk to both food security and rural economies. However, existing literature is notably limited in terms of studies that draw attention to this risk and examine the effects of climate change on tea productivity at a regional scale through rigorous quantitative methods. To this end, this study investigates the influence of climate change on tea productivity in Türkiye’s tea–growing provinces (Artvin, Giresun, Ordu, Rize, and Trabzon) between 2004 and 2022. Distinct from previous studies, we integrate advanced machine learning techniques with the method of moments quantile regression (MMQR) approach to provide comprehensive, reliable, and methodologically robust results for the first time in this context. The results of the MMQR demonstrate that although humidity reduces tea productivity, temperature and precipitation significantly increase it. Furthermore, the results of machine learning research indicate that the tea farming area is the variable with the highest importance, whereas humidity emerges as the least influential factor. These findings indicate that policymakers need to implement integrated agricultural policies in the five tea–growing provinces of the Eastern Black Sea region, including effective moisture management, soil fertility, erosion control, and irrigation infrastructure tailored to the climate and land conditions.

Hypercontractility and Oxidative Stress Drive Creatine Kinase Dysfunction in Hypertrophic Cardiomyopathy

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a prevalent inherited cardiac disorder marked by left ventricular hypertrophy and hypercontractility. This excessive mechanical workload creates an energetic mismatch in which consumption exceeds production, leading to myocardial energy depletion. Although CK (creatine kinase) plays a key role in cardiac energy homeostasis, its involvement in HCM remains unclear. This study investigates how hypercontractility-driven mitochondrial stress and the resulting increase in mitochondrial H 2 O 2 disrupt CK function in HCM. METHODS: CK function was analyzed using myocardial left ventricular tissue from 92 patients with HCM (with and without pathogenic sarcomere variants) and 30 non-failing human controls. Myofilament and mitochondrial CK isoforms were measured using mRNA analysis, protein immunoblotting, enzyme activity assays, mass spectrometry, and redox-sensitive proteomics. To explore links between hypercontractility, mitochondrial reactive oxygen species, and CK dysfunction, we used isolated cardiomyocytes from wild-type, mitochondrial-targeted catalase-overexpressing, CK knockout (myofilament and mitochondrial CK deletion), HCM-associated Mybpc3 knock-in, and mito-roGFP2-Orp1 mouse models. We also tested the effects of the Ca 2+ sensitizer EMD-57033, the CK inhibitor 1-fluoro-2,4-dinitrobenzene (DNFB), and the myosin inhibitor MYK-581, a mavacamten derivative. RESULTS: Our analysis revealed significant reductions in myofilament and mitochondrial CK protein levels, as well as CK activity, in myocardium of patients with HCM, primarily because of oxidative modifications of CK. In isolated mouse cardiomyocytes from wild-type and CK knockouts, hypercontractility induced by EMD-57033 elevated mitochondrial H 2 O 2 , causing cellular arrhythmias and CK inactivation. Hypercontractility-induced oxidative stress, arrhythmias, and CK dysfunction were also observed in Mybpc3 knock-in cardiomyocytes. Mitochondrial-targeted catalase-overexpressing mice with enhanced H 2 O 2 scavenging were protected against H 2 O 2 -induced (EMD-57033-mediated) arrhythmias and CK dysfunction. MYK-581 treatment in Mybpc3 knock-in cardiomyocytes reduced hypercontractility, lowered H 2 O 2 production and arrhythmias, and preserved CK function. CK inhibition using DNFB in wild-type cardiomyocytes elevated mitochondrial H 2 O 2 levels and triggered cellular arrhythmias. This mitochondrial oxidation was independently confirmed in mito-roGFP2-Orp1 cardiomyocytes exposed to DNFB. Mitochondrial-targeted catalase-overexpressing mice were protected from DNFB–induced oxidative stress and arrhythmogenic events. CONCLUSIONS: This study reveals a mechanistic link between hypercontractility, mitochondrial reactive oxygen species, and CK dysfunction in HCM, perpetuating a cycle of energetic dysfunction. Targeting hypercontractility and oxidative stress through myosin inhibition offers a strategy to restore energy balance and reduce arrhythmic risk in HCM.

Lower limb asymmetries in elite junior female vault gymnasts

Genetic and Genomic Testing in Cardiovascular Disease: A Policy Statement From the American Heart Association

The rapid advancement of genomic and precision medicine has expanded the role of genetics and genomics in the diagnosis, risk stratification, and management of cardiovascular diseases. With the decreasing cost and increasing accessibility of genetic testing, its clinical utility continues to expand, necessitating updated policies to ensure equitable access, appropriate regulatory oversight, and ethical data stewardship. This policy statement by the American Heart Association provides a framework addressing key policy areas, including equitable implementation of genetic testing, the impact of federal regulations, data privacy concerns, reimbursement for genetic counseling services, and the integration of emerging technologies such as artificial intelligence in cardiovascular genomics into clinical practice. This policy statement underscores the importance of strategic investments in biobanking and genomic research across all populations to enhance variant interpretation and to improve risk prediction models. In addition, it highlights the evolving landscape of pharmacogenomics, polygenic risk scores, and precision public health approaches to cardiovascular disease prevention. By advocating for a multidisciplinary approach that bridges scientific innovation, clinical application, and policy development, this policy statement aims to optimize the benefits of genetic and genomic testing while mitigating disparities and ethical challenges in its implementation.

Combating cyberbullying with transparency: unveiling the impact of IP location disclosure on cyberbullying in Chinese social media

Troponin Autoantibodies, Macrotroponin, and Assay Interference

Hemolysis-induced hepatic ferroptosis following xenotransfusion of genetically modified pig red blood cells

Abstract To overcome cross-species immunological barriers, researchers utilize gene editing to remove the expression of three major carbohydrate xenoantigens ( α-Gal , Neu5Gc , and Sd(a) ) and insert genes, such as human protective genes ( hCD55 and hCD39 ). This study aimed to investigate the mechanisms underlying long-term hepatic injury following xenotransfusion of genetically modified pig red blood cells (pRBCs). We xenotransfused pRBCs genetically engineered with GGTA1 −/− ( α-Gal −) ; CMAH −/− ( Neu5Gc − ); β4GALNT2 −/− ( Sd(a) − ) ; hCD55; hCD39 into a non-human primate (NHP) model of acute hemorrhage hemolysis and evaluated the long-term immune response to xenogeneic RBCs in the liver, a key organ for RBC metabolism. Immediately after xenotransfusion (D + 1), significant elevations of liver enzymes (AST, ALT) and iron-related factors were observed in the serum levels of the recipients, which were normalized by D + 21. However, long-term analysis revealed excessive accumulation of iron ions in the liver and decreased expression of antioxidant enzymes. The resulting endoplasmic reticulum stress (increased GRP78/BiP expression), lipid peroxide accumulation, and iron-dependent cell death (ferroptosis) persisted in the liver of the recipient. These results suggest that, beyond gene editing, additional hurdles must be overcome to completely block oxidative stress damage caused by impaired RBC lysis. Notably, transcriptomic and immunohistochemical analyses in the NHP model identified the direct role of ferroptosis in xenotransfusion-induced liver injury. Therefore, we propose that a multilayered approach, including blocking the ROS-Iron axis and administering ferroptosis inhibitors, is needed to ensure long-term safety in the clinical development of xenotransfusion.

Hypertrophic Cardiomyopathy is a Disease of Altered Metabolism: Interdependence of Hypercontractility, Oxidative Stress, and Creatine Kinase Dysfunction

Classification of time series using information granules for efficient detection of unmanned aerial vehicles faults

A Storm of Tachycardia Following Stroke: What Is the Mechanism?

Rapid imaging of pulmonary metastasis from colorectal cancer with a red fluorescence probe targeting puromycin-sensitive aminopeptidase and dipeptidyl peptidase IV

Letter by Lei et al Regarding Article, “A Randomized Controlled Trial of Thoracentesis in Acute Heart Failure”

Correction: An axiomatic system engineering design method based on NSGA-II algorithm applied to complex systems

Response by Glargaard and Thune to Letters Regarding Article, “A Randomized Trial of Thoracentesis in Acute Heart Failure”

Effect of hydroquinone as organoelectroactive additive with 1,2,4 triazolium ionic liquid in supercapacitor application

Letter by Harris et al Regarding Article, “A Randomized Controlled Trial of Thoracentesis in Acute Heart Failure”

MCrossFormer: multi-level cross-scale transformer for photovoltaic power and lifespan prediction

Low levels of serum albumin and blood basophils as 10-year mortality predictors in a nationwide Korean COPD cohort

Plant-based diet indices in relation to novel cardiovascular risk factors, major adverse cardiovascular events, and novel anthropometric indices in patients with type 2 diabetes

A speleothem record from the Fertile Crescent covering the last deglaciation better contextualizes neolithization

This study presents a high-resolution, multiproxy (carbon and oxygen isotopes, trace elements, and strontium isotopes) speleothem record from the Kurdistan Region of Iraq extending from the end of the Last Glacial Maximum (LGM) to the Early Holocene (18.0 to 7.5 ka), encompassing the Epipaleolithic–Neolithic transition in the core area of the Fertile Crescent (FC). The record shows that changes in local rainfall amount were coincident with changes in Greenland temperatures, with increased precipitation and enhanced multidecadal hydroclimatic variability during the Bølling–Allerød chronozone, followed by a drier and dustier Younger Dryas. Comparison with regional paleoclimate data suggests similar precipitation patterns across the FC, but with greater hydroclimate variability during the BA and drier conditions during the YD in the eastern sector. Crucially, the record provides a detailed and well-dated paleoenvironmental template by which to contextualize specific cultural events at the subregional scale, as revealed by recent archaeological research on key sites sharing similar environmental settings, allowing to investigate the role of climatic and environmental changes in shaping different neolithization patterns across the FC.