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Background Post‐COVID‐19 symptoms and diseases appeared on many survivors from COVID‐19 which are similar to that of the post‐severe acute respiratory syndrome (SARS) fatigue. Hence, the study aims to investigate and characterise the manifestations which appear after eradication of the coronavirus infection and its relation to disease severity. Method About 287 survivors from COVID‐19 were included in the study, each received a questionnaire divided into three main parts starting from subjects’ demographic data, data about the COVID‐19 status and other comorbidities of the subject, and finally data about post‐COVID‐19 manifestations. Response surface plots were produced to visualise the link between several factors. Results Only 10.8% of all subjects have no manifestation after recovery from the disease while a large percentage of subjects suffered from several symptoms and diseases. The most common symptom reported was fatigue (72.8%), more critical manifestations like stroke, renal failure, myocarditis and pulmonary fibrosis were reported by a few percent of the subjects. There was a relationship between the presence of other comorbidities and severity of the disease. Also, the severity of COVID‐19 was related to the severity of post‐COVID‐19 manifestations. Conclusion The post‐COVID‐19 manifestation is largely similar to the post‐SARS syndrome. All subjects recovered from COVID‐19 should undergo long‐term monitoring for evaluation and treatment of symptoms and conditions that might be precipitated with the new coronavirus infection.

Introduction This study aimed to evaluate the parents’ willingness and attitudes concerning the COVID‐19 vaccine. Method This cross‐sectional study was performed using a self‐administered online survey, covering parents’ and their children's characteristics, parents’ willingness and attitudes towards the COVID‐19 vaccine. A total of 1035 parents participated. Results Analysis showed that 36.3% of parents were willing to have their children receive the COVID‐19 vaccine and that 59.9% were willing to receive it themselves. In addition, 83.9% were willing to have their children vaccinated with the COVID‐19 vaccine if the mortality rates associated with COVID‐19 in children increased following a mutation. After adjusting for significant variables, willingness to receive the COVID‐19 vaccine (AOR = 24.91; 95% CI = 10.93‐56.76), willingness for their children to participate in a COVID‐19 vaccine trial (AOR = 11​.87; 95% CI = 2.41‐58.40] and advising others to receive the COVID‐19 vaccine [AOR = 7.82; 95% CI = 2.50‐24.49] were associated with greater parents’ willingness for their children to receive the COVID‐19 vaccine. Conclusions Parents’ willingness for their children to receive the COVID‐19 vaccine was low. The only characteristics of either parents or children found to affect the parents’ willingness for children to receive the COVID‐19 vaccine was the parents being healthcare workers. Parents’ willingness and positive attitudes towards the COVID‐19 vaccine are factors that increase acceptance of the COVID‐19 vaccine for their children.

Inflammaging, characterized by an increase in low‐grade chronic inflammation with age, is a hallmark of aging and is strongly associated with various age‐related diseases, including chronic liver disease (CLD) and hepatocellular carcinoma (HCC). Because necroptosis is a cell death pathway that induces inflammation through the release of DAMPs, we tested the hypothesis that age‐associated increase in necroptosis contributes to chronic inflammation in aging liver. Phosphorylation of MLKL and MLKL oligomers, markers of necroptosis, as well as phosphorylation of RIPK3 and RIPK1 were significantly upregulated in the livers of old mice relative to young mice and this increase occurred in the later half of life (i.e., after 18 months of age). Markers of M1 macrophages, expression of pro‐inflammatory cytokines (TNFα, IL6 and IL1β), and markers of fibrosis were all significantly upregulated in the liver with age and the change in necroptosis paralleled the changes in inflammation and fibrosis. Hepatocytes and liver macrophages isolated from old mice showed elevated levels of necroptosis markers as well as increased expression of pro‐inflammatory cytokines relative to young mice. Short‐term treatment with the necroptosis inhibitor, necrostatin‐1s (Nec‐1s), reduced necroptosis, markers of M1 macrophages, fibrosis, and cell senescence as well as reducing the expression of pro‐inflammatory cytokines in the livers of old mice. Thus, our data show for the first time that liver aging is associated with increased necroptosis and necroptosis contributes to chronic inflammation in the liver, which in turn appears to contribute to liver fibrosis and possibly CLD. Necroptosis increases with age in the liver and paralleled an increase in the expression of proinflammatory cytokines and markers of fibrosis. Hepatocytes and liver macrophages are the major cell types that undergo necroptosis in the livers of old mice. Short term treatment with the necroptosis inhibitor, necrostatin‐1s (Nec‐1s), reduced necroptosis, expression of proinflammatory cytokines and fibrosis in the livers of old mice.

The increase in senescent cells in tissues, including the brain, is a general feature of normal aging and age‐related pathologies. Senescent cells exhibit a specific phenotype, which includes an altered nuclear morphology and transcriptomic changes. Astrocytes undergo senescence in vitro and in age‐associated neurodegenerative diseases, but little is known about whether this process also occurs in physiological aging, as well as its functional implication. Here, we investigated astrocyte senescence in vitro, in old mouse brains, and in post‐mortem human brain tissue of elderly. We identified a significant loss of lamin‐B1, a major component of the nuclear lamina, as a hallmark of senescent astrocytes. We showed a severe reduction of lamin‐B1 in the dentate gyrus of aged mice, including in hippocampal astrocytes, and in the granular cell layer of the hippocampus of post‐mortem human tissue from non‐demented elderly. The lamin‐B1 reduction was associated with nuclear deformations, represented by an increased incidence of invaginated nuclei and loss of nuclear circularity in senescent astrocytes in vitro and in the aging human hippocampus. We also found differences in lamin‐B1 levels and astrocyte nuclear morphology between the granular cell layer and polymorphic layer in the elderly human hippocampus, suggesting an intra‐regional‐dependent aging response of human astrocytes. Moreover, we described senescence‐associated impaired neuritogenic and synaptogenic capacity of mouse astrocytes. Our findings show that reduction of lamin‐B1 is a conserved feature of hippocampal cells aging, including astrocytes, and shed light on significant defects in nuclear lamina structure which may contribute to astrocyte dysfunctions during aging. Aging is associated with lamin‐B1 loss in senescent astrocytes in vitro and neural cells, including astrocytes, in the aging mouse and human hippocampus. The lamin‐B1 reduction was linked to senescence‐related molecular and functional changes and nuclear deformations, represented by an increased incidence of invaginated nuclei and reduced nuclear circularity in senescent astrocytes in vitro and in the mouse and human hippocampal aging.

Aging is a strong risk factor for many chronic diseases. However, the impact of an aging population on the prevalence of chronic diseases and related healthcare costs are not known. We used a prevalence‐based approach that combines accurate clinical and drug prescription data from Health Search CSD‐LPD. This is a longitudinal observational data set containing computer‐based patient records collected by Italian general practitioners (GP) and up‐to‐date healthcare expenditures data from the SiSSI Project. The analysis is based on data collected by 900 GP on an unbalanced sample of more than 1 million patients aged 35+, observed in different time periods between 2005 and 2014. In 2014, 86% of the Italian adults older than 65 had at least one chronic condition, and 56.7% had two or more. Prevalence of multiple chronic diseases and healthcare utilization increased among older and younger adults between 2004 and 2014. Indeed, in the last 10 years, average number of prescriptions increased by approximately 26%, while laboratory and diagnostic tests by 27%. The average number of DDD prescribed increased with age in all the observed years (from 114 in 2005 to 119.9 in 2014 for the 35–50 age group and from 774.9 to 1,178.1 for the 81+ patients). The alarming rising trends in the prevalence of chronic disease and associated healthcare costs in Italy, as well as in many other developed countries, call for an urgent implementation of interventions that prevent or slow the accumulation of metabolic and molecular damage associated with multiple chronic disease.

Frailty is a common geriatric syndrome and strongly associated with disability, mortality and hospitalization. Frailty is commonly measured using the frailty index (FI), based on the accumulation of a number of health deficits during the life course. The mechanisms underlying FI are multifactorial and not well understood, but a genetic basis has been suggested with heritability estimates between 30 and 45%. Understanding the genetic determinants and biological mechanisms underpinning FI may help to delay or even prevent frailty. We performed a genome‐wide association study (GWAS) meta‐analysis of a frailty index in European descent UK Biobank participants (n = 164,610, 60–70 years) and Swedish TwinGene participants (n = 10,616, 41–87 years). FI calculation was based on 49 or 44 self‐reported items on symptoms, disabilities and diagnosed diseases for UK Biobank and TwinGene, respectively. 14 loci were associated with the FI (p < 5*10−8). Many FI‐associated loci have established associations with traits such as body mass index, cardiovascular disease, smoking, HLA proteins, depression and neuroticism; however, one appears to be novel. The estimated single nucleotide polymorphism (SNP) heritability of the FI was 11% (0.11, SE 0.005). In enrichment analysis, genes expressed in the frontal cortex and hippocampus were significantly downregulated (adjusted p < 0.05). We also used Mendelian randomization to identify modifiable traits and exposures that may affect frailty risk, with a higher educational attainment genetic risk score being associated with a lower degree of frailty. Risk of frailty is influenced by many genetic factors, including well‐known disease risk factors and mental health, with particular emphasis on pathways in the brain. This genome‐wide association study meta‐analysis of the frailty index (FI) in UK Biobank and TwinGene, identified 14 loci associated with the FI. Many FI‐associated loci have established associations with well‐known disease risk factors such as BMI, cardiovascular disease, smoking, HLA proteins, depression and neuroticism. However 1 was novel. Risk of frailty is influenced by many genetic factors, including well‐known disease risk factors and mental health, with particular emphasis on pathways in the brain.

Aging leads to increased cellular senescence and is associated with decreased potency of tissue‐specific stem/progenitor cells. Here, we have done an extensive analysis of cardiac progenitor cells (CPCs) isolated from human subjects with cardiovascular disease, aged 32–86 years. In aged subjects (>70 years old), over half of CPCs are senescent (p16INK4A, SA‐β‐gal, DNA damage γH2AX, telomere length, senescence‐associated secretory phenotype [SASP]), unable to replicate, differentiate, regenerate or restore cardiac function following transplantation into the infarcted heart. SASP factors secreted by senescent CPCs renders otherwise healthy CPCs to senescence. Elimination of senescent CPCs using senolytics abrogates the SASP and its debilitative effect in vitro. Global elimination of senescent cells in aged mice (INK‐ATTAC or wild‐type mice treated with D + Q senolytics) in vivo activates resident CPCs and increased the number of small Ki67‐, EdU‐positive cardiomyocytes. Therapeutic approaches that eliminate senescent cells may alleviate cardiac deterioration with aging and restore the regenerative capacity of the heart.

Objective In this study, we aim to investigate the thoughts and attitudes of individuals towards the future COVID‐19 vaccine. Methods This descriptive study was carried out on the web between 10/06/2020 and 10/07/2020. The sample constitutes all individuals above 18 years of age using social media and smartphone. The e‐survey form was shared by the researchers via the web for a month, and those who completed the survey were included in the study and formed the sample of the research. Results Seven‐hundred and fifty‐nine people participated. 49.7% of the participants stated to be vaccinated; 38.4% of them stated to be vaccinated their children against COVID‐19; if the vaccine for COVID‐19 is developed. The request for the COVID‐19 vaccine had relationship with gender, occupation, health insurance, anxiety level, having children and willing to get vaccinated for their children. “Afraid of the side effects of vaccine”, “don't think it can be reliable as it will be a new vaccine” and “COVID‐19 infection is a biological weapon and the vaccine will serve those who produce this virus” were the most common reasons for rejection of vaccine. Conclusion In our study, afraid of the side effects of vaccine and not thinking it can be reliable as it will be a new vaccine are the most reasons of indecision and rejection about COVID 19 vaccine. In order for the future COVID 19 vaccination campaign to not fail, media, politicians and healthcare professionals should closely follow the vaccination development processes, inform the public transparently and consider public's concerns.

Background In the telepharmacy model, the pharmacist can play a pivotal role in delivering pharmaceutical services for patients. However, evidence of pharmacists’ impact on improving patient outcomes through disease outbreak through telepharmacy is sparse. Objectives This study aims to examine pharmacists' attitudes towards clinical benefits and identify challenges regarding the use of telepharmacy during the COVID‐19 pandemic in Jordan. Method A cross‐sectional survey design was used to recruit eligible participants from both hospital and community pharmacies. Results A total of 364 pharmacists agreed to participate in the study. The majority of the participants (70.6%) expressed favourable attitudes towards telepharmacy to accurately capture and report signs and symptoms of COVID‐19. Almost 91% agreed that patients can receive immediate medical feedback while using telepharmacy services. Pharmacists (87%) emphasised their role in the monitoring of physiological parameters when entered by patients using telepharmacy technology. However, more than half of the participants reported that lack of reimbursement and evidence‐based studies might hinder the use of telemedicine technology to deliver remote clinical services. Conclusion The need for implementing telepharmacy technology has been further boosted because of its noticeable benefits in promoting convenient healthcare services remotely in emergency situations.

Several biomarkers of healthy aging have been proposed in recent years, including the epigenetic clocks, based on DNA methylation (DNAm) measures, which are getting increasingly accurate in predicting the individual biological age. The recently developed “next‐generation clock” DNAmGrimAge outperforms “first‐generation clocks” in predicting longevity and the onset of many age‐related pathological conditions and diseases. Additionally, the total number of stochastic epigenetic mutations (SEMs), also known as the epigenetic mutation load (EML), has been proposed as a complementary DNAm‐based biomarker of healthy aging. A fundamental biological property of epigenetic, and in particular DNAm modifications, is the potential reversibility of the effect, raising questions about the possible slowdown of epigenetic aging by modifying one's lifestyle. Here, we investigated whether improved dietary habits and increased physical activity have favorable effects on aging biomarkers in healthy postmenopausal women. The study sample consists of 219 women from the “Diet, Physical Activity, and Mammography” (DAMA) study: a 24‐month randomized factorial intervention trial with DNAm measured twice, at baseline and the end of the trial. Women who participated in the dietary intervention had a significant slowing of the DNAmGrimAge clock, whereas increasing physical activity led to a significant reduction of SEMs in crucial cancer‐related pathways. Our study provides strong evidence of a causal association between lifestyle modification and slowing down of DNAm aging biomarkers. This randomized trial elucidates the causal relationship between lifestyle and healthy aging‐related epigenetic mechanisms. In a 24‐month randomized factorial intervention trial, dietary and physical activity interventions slowed down DNA methylation‐based biomarkers of aging.