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Sarcopenia, an age-related decline in skeletal muscle mass, strength, and function, is increasingly recognized as a significant condition in the aging population, particularly among those with cardiovascular diseases (CVD). This review provides a comprehensive synthesis of the interplay between sarcopenia and cardiogeriatrics, emphasizing shared mechanisms such as chronic low-grade inflammation (inflammaging), hormonal dysregulation, oxidative stress, and physical inactivity. Despite advancements in diagnostic frameworks, such as the EWGSOP2 and AWGS definitions, variability in criteria and assessment methods continues to challenge standardization. Key diagnostic tools include dual-energy X-ray absorptiometry (DXA) and bioimpedance analysis (BIA) for muscle mass, alongside functional measures such as grip strength and gait speed. The review highlights the bidirectional relationship between sarcopenia and cardiovascular conditions such as heart failure, aortic stenosis, and atherosclerotic cardiovascular disease, which exacerbate each other through complex pathophysiological mechanisms. Emerging therapeutic strategies targeting the mTOR pathway, NAD+ metabolism, and senescence-related processes offer promise in mitigating sarcopenia's progression. Additionally, integrated interventions combining resistance training, nutritional optimization, and novel anti-aging therapies hold significant potential for improving outcomes. This paper underscores critical gaps in the evidence, including the need for longitudinal studies to establish causality and the validation of advanced therapeutic approaches in clinical settings. Future research should leverage multi-omics technologies and machine learning to identify biomarkers and personalize interventions. Addressing these challenges is essential to reducing sarcopenia's burden and enhancing the quality of life for elderly individuals with comorbid cardiovascular conditions. This synthesis aims to guide future research and promote effective, individualized management strategies. [ABSTRACT FROM AUTHOR]

Heart failure (HF) remains a major cause of morbidity and mortality worldwide. While standard treatments primarily target neurohormonal pathways, emerging evidence highlights the significant role of hormonal deficiencies, such as impaired growth hormone (GH) signaling, in HF progression and outcomes. GH is crucial for cardiovascular and skeletal muscle function, and its deficiency has been associated with worse prognosis. This review synthesizes recent findings from randomized controlled trials (RCTs) to explore how GH can contribute to personalized care and improve patient stratification in HF. A comprehensive literature review was conducted using PubMed up to 10 October 2024. Search terms included "growth hormone" combined with "heart failure", "HFrEF", "HFpEF", and "HFmrEF." Only placebo-controlled RCTs published in English and involving human subjects were considered. Data on study design, participant characteristics, GH dosing, and key clinical outcomes were systematically extracted and analyzed. Several trials demonstrated that GH therapy can transiently improve left ventricular ejection fraction (LVEF), exercise capacity, and reduce inflammatory markers. For example, one study has reported an increase in LVEF from 32 ± 3.8% to 43.8 ± 4.6% (p = 0.002), following three months of GH therapy in post-MI HF patients. However, benefits diminished after discontinuation. Additional studies have observed sustained improvements in peak oxygen consumption and LVEF over four years, with an additional trend towards hard endpoint improvement. Conversely, some studies showed no significant impact on cardiac function, highlighting heterogeneity in outcomes. As a result, GH therapy holds promise for improving cardiac and functional parameters in HF patients, but evidence remains mixed. Larger, long-term RCTs are needed to confirm its efficacy and safety. Precision medicine approaches and biomarker-driven strategies may optimize patient outcomes and guide clinical practice. [ABSTRACT FROM AUTHOR]

Background: Cardiometabolic heart failure with preserved ejection fraction (HFpEF) is largely driven by obesity-related factors, including adipokines and bioactive peptides primarily secreted by the adipose tissue, such as leptin, adiponectin, and resistin. These molecules link metabolic dysregulation to cardiovascular dysfunction, influencing HFpEF progression and patient outcomes Methods: A comprehensive literature search was conducted in PubMed up to 20 November 2024, using keywords and MeSH terms, such as "HFpEF", "adipokines", "leptin", "adiponectin", and "resistin", yielding 723 results. Boolean operators refined the search, and reference lists of key studies were reviewed. After screening for duplicates and irrelevant studies, 103 articles were included, providing data on adipokines' roles in HFpEF pathophysiology, biomarkers, and therapeutic implications. Results: Both preclinical and clinical studies have demonstrated that adipokines play a role in modulating cardiovascular function, thereby contributing to the development of cardiometabolic HFpEF. Leptin promotes myocardial hypertrophy, fibrosis, endothelial dysfunction, and inflammation, though contradictory evidence suggests potential cardioprotective roles in subgroups like obese African American women. Adiponectin generally offers protective effects but presents a paradox, where elevated levels may correlate with worse outcomes, which may reflect either a compensatory response to cardiac dysfunction or a maladaptive state characterized by adiponectin resistance. Resistin is associated with increased cardiovascular risk through pro-inflammatory and pro-fibrotic effects, though its role in HFpEF requires further clarification. Other adipokines, like retinol-binding protein 4 and omentin-1, have emerged as potential contributors. Despite growing insights, clinical translation remains limited, underscoring a significant gap between experimental evidence and therapeutic application. Conclusions: Future research should focus on targeted interventions that modulate adipokine pathways to potentially improve HFpEF outcomes. Innovative treatment strategies addressing underlying metabolic disturbances and adipokine dysregulation are essential for advancing the management of this challenging condition. [ABSTRACT FROM AUTHOR]

Background: As the population ages, the prevalence of surgical interventions in individuals aged 65+ continues to increase. This poses unique challenges due to the higher incidence of comorbidities, polypharmacy, and frailty in the elderly population, which result in high peri-operative risks. Traditional preoperative risk assessment tools often fail to accurately predict post-operative outcomes in the elderly, overlooking the complex interplay of factors that contribute to risk in the elderly. Methods: A literature review was conducted, focusing on the predictive value of CGA for postoperative prognosis and the implementation of perioperative interventions. Results: Evidence shows that CGA is a superior predictive tool compared to traditional models, as it more accurately identifies elderly patients at higher risk of complications such as postoperative delirium, infections, and prolonged hospital stays. CGA includes assessments of frailty, sarcopenia, nutritional status, cognitive function, mental health, and functional status, which are crucial in predicting post-operative outcomes. Studies demonstrate that CGA can also guide personalized perioperative care, including nutritional support, physical training, and mental health interventions, leading to improved surgical outcomes and reduced functional decline. Conclusions: The CGA provides a more holistic approach to perioperative risk assessment in elderly patients, addressing the limitations of traditional tools. CGA can help guide surgical decisions (e.g., curative or palliative) and select the profiles of patients that will benefit from perioperative interventions to improve their prognosis and prevent functional decline. [ABSTRACT FROM AUTHOR]

This study investigates the forecasting of cardiovascular mortality trends in Greece’s elderly population. Utilizing mortality data from 2001 to 2020, we employ two forecasting models: the Autoregressive Integrated Moving Average (ARIMA) and Facebook's Prophet model. Our study evaluates the efficacy of these models in predicting cardiovascular mortality trends over 2020-2030. The ARIMA model showcased predictive accuracy for the general and male population within the 65-79 age group, whereas the Prophet model provided better forecasts for females in the same age bracket. Our findings emphasize the need for adaptive forecasting tools that accommodate demographic-specific characteristics and highlight the role of advanced statistical methods in health policy planning. [ABSTRACT FROM AUTHOR]

Background: It is now realized that Parkinson's disease (PD) pathology extends beyond the substantia nigra, affecting both central and peripheral nervous systems, and exhibits a variety of non-motor symptoms often preceding motor features. Neuroinflammation induced by activated microglia and astrocytes is thought to underlie these manifestations. α-Synuclein aggregation has been linked with sustained neuroinflammation in PD, aggravating neuronal degeneration; however, there is still a lack of critical information about the structural identity of the α-synuclein conformers that activate microglia and/or astrocytes and the molecular pathways involved. Methods: To investigate the role of α-synuclein conformers in the development and maintenance of neuroinflammation, we used primary quiescent microglia and astrocytes, post-mortem brain tissues from PD patients and A53T α-synuclein transgenic mice that recapitulate key features of PD-related inflammatory responses in the absence of cell death, i.e., increased levels of pro-inflammatory cytokines and complement proteins. Biochemical and -omics techniques including RNAseq and secretomic analyses, combined with 3D reconstruction of individual astrocytes and live calcium imaging, were used to uncover the molecular mechanisms underlying glial responses in the presence of α-synuclein oligomers in vivo and in vitro. Results: We found that the presence of SDS-resistant hyper-phosphorylated α-synuclein oligomers, but not monomers, was correlated with sustained inflammatory responses, such as elevated levels of endogenous antibodies and cytokines and microglial activation. Similar oligomeric α-synuclein species were found in post-mortem human brain samples of PD patients but not control individuals. Detailed analysis revealed a decrease in Iba1Low/CD68Low microglia and robust alterations in astrocyte number and morphology including process retraction. Our data indicated an activation of the p38/ATF2 signaling pathway mostly in microglia and a sustained induction of the NF-κB pathway in astrocytes of A53T mice. The sustained NF-κB activity triggered the upregulation of astrocytic T-type Cav3.2 Ca2+ channels, altering the astrocytic secretome and promoting the secretion of IGFBPL1, an IGF-1 binding protein with anti-inflammatory and neuroprotective potential. Conclusions: Our work supports a causative link between the neuron-produced α-synuclein oligomers and sustained neuroinflammation in vivo and maps the signaling pathways that are stimulated in microglia and astrocytes. It also highlights the recruitment of astrocytic Cav3.2 channels as a potential neuroprotective mediator against the α-synuclein-induced neuroinflammation. [ABSTRACT FROM AUTHOR]

A broadband coplanar waveguide (CPW) to coplanar strip (CPS) transmission line transition directly integrated with an RF microelectromechanical systems reconfigurable multiband antenna is presented in this paper. This transition design exhibits very good performance up to 55 GHz, and uses a minimum number of dissimilar transmission line sections and wire bonds, achieving a low-loss and low-cost balancing solution to feed planar antenna designs. The transition design methodology that was followed is described and measurement results are presented. Index Terms--Antenna feed, coplanar strip (CPS), coplanar stripline, coplanar waveguide (CPW), transition.

Devices and systems that use RF microelectro-mechanical systems (RF MEMS) switching elements typically use one switch topology. The switch is designed to meet all of the performance criteria. However, this can be limiting for highly dynamic applications that require a great deal of reconfigurability. In this paper, three sets of RF MEMS switches with different actuation voltages are used to sequentially activate and deactivate parts of a multiband Sierpinski fractal antenna. The implementation of such a concept allows for direct actuation of the electrostatic MEMS switches through the RF signal feed, therefore eliminating the need for individual switch dc bias lines. This reconfigurable antenna was fabricated on liquid crystal polymer substrate and operates at several different frequencies between 2.4 and 18 GHz while maintaining its radiation characteristics. It is the first integrated RF MEMS reconfigurable antenna on a flexible organic polymer substrate for multiband antenna applications. Simulation and measurement results are presented in this paper to validate the proposed concept. [2007-0013] Index Terms--Liquid crystal polymer (LCP), multiband, reconfigurable antenna, RF microelectromechanical systems (RF MEMS), Sierpinski fractal antenna.

Reconfigurability in an antenna system is a desired characteristic that has been the focus of much research in recent years. In this work, ohmic contact cantilever RF-MEMS switches are integrated with self-similar planar antennas to provide a reconfigurable antenna system that radiates similar patterns over a wide range of frequencies. The different issues encountered during the integration of the MEMS switches and the overall system design procedure are described herein. The final model radiates at three widely separated frequencies with very similar radiation patterns. The proposed concept can be extended to reconfigurable linear antenna arrays or to more complex antenna structures with large improvements in antenna performance. Index Terms--Fractal, reconfigurable antennas, RF-MEMS, self-similar, Sierpinski, silicon.

Procedures using neural networks are developed for characterizing multiband reconfigurable antennas. A multilayer perceptron (MLP) is used to locate the operational frequency bands of the antenna at different reconfigured conditions. Another self-organizing map (SOM) neural network accomplishes the task of locating the switches to be turned ON for a desired frequency response. The developed formulation is tested on a laboratory prototype antenna. Index Terms--Multilayer perceptron (MLP), neural networks, reconfigurable antenna, self-organizing map (SOM).

In recent years, the art of using neural networks (NNs) for wireless-communication engineering has been gaining momentum. Although it has been used for a variety of purposes and in different ways, the basic purpose of applying neural networks is to change from the lengthy analysis and design cycles required to develop high-performance systems to very short product-development times. This article overviews the current state of research in this area. Different applications of neural-network techniques for wireless communication front ends are briefly reviewed, stressing the purpose and the way neural networks have been implemented, followed by a description of future avenues of research in this field. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Methods Results Conclusions Ghrelin is emerging as a promising therapeutic option for heart failure (HF) due to its potent inotropic, anabolic, and cardioprotective properties. This review aims to critically examine the available clinical evidence on ghrelin therapy in HF, while also incorporating key findings from preclinical studies that support its therapeutic potential.A comprehensive search was conducted in PubMed and the Cochrane Library up to September 15, 2024, using the keywords “heart failure” and “ghrelin.” From 247 identified records, four randomized controlled trials, one open‐label trial, one observational study, and key preclinical studies were included. Two independent authors performed the screening and quality assessment, with any discrepancies resolved through consensus.Clinical trials investigating ghrelin's acute effects in HF patients have demonstrated significant improvements in cardiac output, ranging from 15% to 30%. Moreover, one study showed that a 3‐week course of ghrelin therapy significantly increased maximal oxygen consumption, lean body mass, and grip strength in HF patients. Preclinical studies further support these clinical findings, highlighting additional benefits of ghrelin, including modulation of the autonomic nervous system, promotion of vasodilation, enhancement of endothelial function, prevention of myocardial remodeling, reduction of arrhythmogenic risk, and increased muscle mass in HF models.Ghrelin is a promising therapeutic option for HF, particularly as an inotropic agent with multifaceted benefits, including autonomic nervous system modulation, anabolic effects, and metabolic regulation. However, further trials are required to confirm its long‐term efficacy and safety and assess whether its benefits can translate into reductions in hard clinical endpoints. [ABSTRACT FROM AUTHOR]

Context: Guideline-directed medical therapy of heart failure (HF) primarily targets neurohormonal activation. However, growth hormone (GH) has emerged as a potential treatment for the multiple hormonal deficiency syndrome, which is associated with worse outcomes in HF., Objective: This study evaluates the efficacy and safety of GH therapy in HF., Data Sources: A systematic search was conducted in PubMed, Cochrane Library, and ClinicalTrials.gov, according to PRISMA guidelines., Study Selection: Randomized, placebo-controlled trials studying GH therapy in adult HF patients were included. Of the 1,184 initially identified records, 17 studies (1.4%) met the inclusion criteria., Data Extraction: Two independent authors conducted the search, with any disagreements resolved by a third author. Study quality was assessed using predefined criteria, including randomization, blinding, and the presence of a placebo group., Data Synthesis: A random-effects model was applied due to heterogeneity across studies. GH therapy significantly improved left ventricular ejection fraction (3.34%, 95% CI: 1.09% to 5.59%, p=0.0037), peak oxygen consumption (2.84 mL/kg/min, 95% CI: 1.32 mL/kg/min to 4.36 mL/kg/min, p=0.0002), and New York Heart Association class (-0.44, 95% CI: -0.08 to -0.81, p=0.023). GH therapy also reduced the composite of death, worsening HF or ventricular tachycardia by 41% (95% CI: 0.39-0.90, p=0.013). Subgroup analyses indicated that patients with ischemic cardiomyopathy, baseline ejection fraction ≥30% and longer treatment duration experienced greater benefits., Conclusions: GH therapy may improve cardiac function, exercise capacity, and HF symptoms, with a trend towards improvement in hard endpoints, such as worsening HF. Event-driven trials are necessary to validate these findings., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.)