Alfordcarrillo1433

The 2019-2020 SARS-related coronavirus-2 (SARS-CoV-2) pandemic has brought unprecedented challenges to healthcare sectors around the world. As of November 2020, there have been over 64 million confirmed cases and approaching 2 million deaths globally. Despite the large number of positive cases, there are very limited established standards of care and therapeutic options available. To date, there is still no Food and Drug Administration (FDA) approved vaccine for COVID-19, although there are several options in various clinical trial stages. Herein, we have performed a global review evaluating the roles of age and sex on COVID-19 hospitalizations, ICU admissions, deaths in hospitals, and deaths in nursing homes. We have identified a trend in which elderly and male patients are significantly affected by adverse outcomes. There is evidence suggesting that sex hormone levels can influence immune system function against SARS-CoV-2 infection, thus reducing the adverse effects of COVID-19. Since older adults have lower levels of these sex hormones, we therefore speculate, within rational scientific context, that sex steroids, such as estrogen and progesterone, needs further consideration for use as alternative therapeutic option for treating COVID-19 elderly patients. To our knowledge, this is the first comprehensive article evaluating the significance of sex hormones in COVID-19 outcomes in older adults.Worldwide COVID-19 infection poses an enormous risk to public health and an alarming global socioeconomic burden. The impact of the COVID-19 pandemic on individuals with underlying health conditions as well as on the elderly population is extensive and effective strategies are needed to understand the mechanism behind it. Cellular senescence defines as an irreversible cell cycle arrest due to DNA damage leading to accumulation of senescent cells in the elderly population and may result in worsening of COVID-19 mediated increased mortality. However, whether this variation in senescence levels, in different aged populations, translation to COVID-19 infection is unknown. The spike protein of SARS-CoV-2 has been recently identified to be responsible for inducing pathogenic signals, although a clear understanding of how the host receptor interacts with SARS-CoV-2 protein and mediates the immune responses is not clear. In this review, we address the epidemiology of SARS-CoV-2 and the cellular senescence responding immune response to pathogenic SARS-CoV-2. We provide a prospective summary of what to expect and how to brace the possible immunological strategy to protect against COVID-19 infection. The review majorly explores an underline mechanism of how senescent cells trigger a hyperimmune inflammatory response and cause high mortality in aging people could serve as a potential aid to alleviate the treatment for elderly battling COVID-19 infection.Metabolomics is the latest state-of-the-art omics technology that provides a comprehensive quantitative profile of metabolites. The metabolites are the cellular end products of metabolic reactions that explain the ultimate response to genomic, transcriptomic, proteomic, or environmental changes. Aging is a natural inevitable process characterized by a time-dependent decline of various physiological and metabolic functions and are dominated collectively by genetics, proteomics, metabolomics, environmental factors, diet, and lifestyle. The precise mechanism of the aging process is unclear, but the metabolomics has the potential to add significant insight by providing a detailed metabolite profile and altered metabolomic functions with age. Although the application of metabolomics to aging research is still relatively new, extensive attempts have been made to understand the biology of aging through a quantitative metabolite profile. This review summarises recent developments and up-to-date information on metabolomics studies in aging research with a major emphasis on aging biomarkers in less invasive biofluids. The importance of an integrative approach that combines multi-omics data to understand the complex aging process is discussed. Despite various innovations in metabolomics and metabolite associated with redox homeostasis, central energy pathways, lipid metabolism, and amino acid, a major challenge remains to provide conclusive aging biomarkers.Frailty is a condition characterized by a high vulnerability to low-power stressor. Frailty increases with age and is associated with higher complications and mortality. Several indexes have been used to quantify frailty. Spine diseases, both degenerative and oncologic, frequently require surgery which is related to complications and mortality. Aim of the present systematic review was to collect the most frequently used frailty indexes in clinics to predict surgical outcomes in patients affected by spine diseases, taking into account gender differences. Three databases were employed, and 29 retrospective clinical studies were included in this systematic review. The identified spine pathologies were primary and metastatic spine tumors, adult spine deformity (ASD), degenerative spine disease (DSD), cervical deformity (CD) and other pathologies that affected lumbar spine or multiple spine levels. Eleven indexes were identified modified Frailty Index (mFI), Adult spinal deformity frailty index (ASD-FI), mFI-5, Metastatic Spinal Tumor Frailty Index (MSTFI), Fried criteria, Cervical deformity frailty index (CD-FI), Spinal tumor frailty index (STFI), Frailty Phenotype criteria (FP), Frailty Index (FI), FRAIL scale and Modified CD-FI (mCD-FI). All these indexes correlated well with minor and major postoperative complications, mortality and length of stay in hospital. Results on gender differences and frailty are still conflicting, although few studies show that women are more likely to develop frailty and more complications in the post-operative period than men. This systematic review could help the surgeon in the adoption of frailty indexes, before the operation, and in preventing complications in frail patients.The global population is aging and the demand for critical care wards increasing. Aging is associated not only with physiological and cognitive vulnerability, but also with a decline in organ function. A new topic in geriatric care is how to appropriately use critical care resources and provide the best treatment plan for very old patients (VOPs). Our special geriatric intensive care unit has admitted nearly 500 VOPs. In this review, we share our VOP treatment strategy and summarize the key points as "ABCCDEFGHI bundles." The aim is to help intensivists to provide more comprehensive therapy for VOPs in intensive care units.In recent decades, the incidence and diagnosis of thyroid cancer have risen dramatically, and thyroid cancer has now become the most common endocrine cancer in the world. The onset of thyroid cancer is insidious, and its progression is slow and difficult to detect. Pirfenidone Smad inhibitor Therefore, early prevention and treatment have important strategic significance. Moreover, an in-depth exploration of the pathogenesis of thyroid cancer is key to early prevention and treatment. Substantial evidence supports obesity as an independent risk factor for thyroid cancer. Adipose tissue dysfunction in the obese state is accompanied by dysregulation of a variety of adipocytokines. Adiponectin (APN) is one of the most pivotal adipocytokines, and its connection with obesity and obesity-related disease has gradually become a hot topic in research. Recently, the association between APN and thyroid cancer has received increasing attention. The purpose of this review is to systematically review previous studies, give prominence to APN, focus on the relationship between APN, obesity and thyroid cancer, and uncover the underlying pathogenic mechanisms.Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common sleep disorder, negatively influencing individuals' quality of life and socioeconomic burden. In recent years, OSAHS has been reported in not only constituting an aging-associated disease, but also in accelerating and/or potentiating aging mechanisms. However, the negative impacts of OSAHS on aging are underestimated because of low level of public awareness about this disease and high rates of undiagnosed cases, which are more critical in developing countries or economically disadvantaged regions. Hence, reviewing previously reported observations may assist scholars to better indicate that OSAHS is likely a novel potential risk for aging. Further understanding of the pathophysiological mechanism of OSAHS and its role in procession of aging may markedly highlight the importance of this common sleep disorder.Stroke is a leading cause of disability and mortality all over the world. Due to an aging population, the incidence of stroke is rising significantly, which has led to devastating consequences for patients. In addition to traditional risk factors such as age, hypertension, hyperlipidemia, diabetes and atrial fibrillation, sleep disorders, as independent modifiable risk factors for stroke, have been highlighted increasingly. In this review, we provide an overview of common types of current sleep disturbances in cerebrovascular diseases, including insomnia, hypersomnia, breathing-related sleep disorders, and parasomnias. Moreover, evidence-based clinical therapeutic strategies and pitfalls of specific sleep disorders after stroke are discussed. We also review the neurobiological mechanisms of these treatments as well as their effects on stroke. Since depression after stroke is so prevalent and closely related to sleep disorders, treatments of post-stroke depression are also briefly mentioned in this review article.Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. link2 This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.Iron is an essential component in many biological processes in the human body. It is critical for the visual phototransduction cascade in the retina. However, excess iron can be toxic. Iron accumulation and reduced efficiency of intracellular antioxidative defense systems predispose the aging retina to oxidative stress-induced cell death. Age-related macular degeneration (AMD) is characterized by retinal iron accumulation and lipid peroxidation. The mechanisms underlying AMD include oxidative stress-mediated death of retinal pigment epithelium (RPE) cells and subsequent death of retinal photoreceptors. link3 Understanding the mechanism of the disruption of iron and redox homeostasis in the aging retina and AMD is crucial to decipher these mechanisms of cell death and AMD pathogenesis. The mechanisms of retinal cell death in AMD are an area of active investigation; previous studies have proposed several types of cell death as major mechanisms. Ferroptosis, a newly discovered programmed cell death pathway, has been associated with the pathogenesis of several neurodegenerative diseases.