A Crucial Role for Antimicrobial Stewardship in the Midst of COVID-19

As the world deals with a pandemic, there remains another global challenge that cannot be ignored. Use of broad-spectrum antibiotics may be justified, as we are trying to treat a novel disease condition, which, in turn, could lead to an increase in antimicrobial resistance. We can decrease morbidity, mortality, and health care costs by controlling antimicrobial resistance, but it requires antimicrobial stewardship. Major components of effective and timely antimicrobial stewardship are diagnostic stewardship, infection prevention and control, and integration of COVID-19-specific flags into electronic health records, all of which may be integrated into current strategies of COVID-19 mitigation and management. Going through the influenza season of 2020, implementation of antimicrobial stewardship education efforts in the United States can help us contend with influenza in addition to COVID-19 and any bacterial coinfections or secondary infections. Additional solutions include the development of vaccines, alternative therapies, such as antibodies, and advanced diagnostics using advances in genomics and computer science

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

From Frontiers via Jisc Publications RouterHistory: collection 2021, received 2021-04-13, accepted 2021-05-10, epub 2021-06-21Publication status: PublishedThe incidence of heart failure (HF) continues to increase rapidly in patients with diabetes. It is marked by myocardial remodeling, including fibrosis, hypertrophy, and cell death, leading to diastolic dysfunction with or without systolic dysfunction. Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in the absence of coronary artery disease. DCM is partially induced by chronic systemic inflammation, underpinned by a hostile environment due to hyperglycemia, hyperlipidemia, hyperinsulinemia, and insulin resistance. The detrimental role of leukocytes, cytokines, and chemokines is evident in the diabetic heart, yet the precise role of inflammation as a cause or consequence of DCM remains incompletely understood. Here, we provide a concise review of the inflammatory signaling mechanisms contributing to the clinical complications of diabetes-associated HF. Overall, the impact of inflammation on the onset and development of DCM suggests the potential benefits of targeting inflammatory cascades to prevent DCM. This review is tailored to outline the known effects of the current anti-diabetic drugs, anti-inflammatory therapies, and natural compounds on inflammation, which mitigate HF progression in diabetic populations

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

The incidence of heart failure (HF) continues to increase rapidly in patients with diabetes. It is marked by myocardial remodeling, including fibrosis, hypertrophy, and cell death, leading to diastolic dysfunction with or without systolic dysfunction. Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in the absence of coronary artery disease. DCM is partially induced by chronic systemic inflammation, underpinned by a hostile environment due to hyperglycemia, hyperlipidemia, hyperinsulinemia, and insulin resistance. The detrimental role of leukocytes, cytokines, and chemokines is evident in the diabetic heart, yet the precise role of inflammation as a cause or consequence of DCM remains incompletely understood. Here, we provide a concise review of the inflammatory signaling mechanisms contributing to the clinical complications of diabetes-associated HF. Overall, the impact of inflammation on the onset and development of DCM suggests the potential benefits of targeting inflammatory cascades to prevent DCM. This review is tailored to outline the known effects of the current anti-diabetic drugs, anti-inflammatory therapies, and natural compounds on inflammation, which mitigate HF progression in diabetic populations

Sosialisasi Stunting dan Pencegahan Stunting Era New Normal di Kelurahan Tampan Kota Pekanbaru

Stunting is a chronic malnutrition problem caused by inadequate nutritional intake for a long time due to feeding that is not in accordance with nutritional needs. The purpose of this activity is to add insight to parents in choosing nutritious foods to avoid stunting. The existence of stunting prevention socialization can help the community to change their lifestyle for the better. The implementation of this Stunting Prevention program is carried out using a participatory approach, meaning that the fostered partners will be actively involved in every stage and coaching activities carried out through introduction and education about stunting, behavior education clean and healthy living, followed by the provision of additional food for toddlers, pregnant women, and children affected by stunting. Some of the steps we take in preventing stunting in the Tampan Village are: 1. Survey and data search, 2. Socialization and education on stunting, 3. Education on clean and healthy living behavior, 4. Provision of additional food. Stunting is a dangerous disease condition and must be continuously considered by the community and the government. If it is not continued, it is feared that Indonesia will experience a Lost Generation crisis. The Kukerta Team of the University of Riau took the initiative and intensified this stunting prevention program, as a form of concern for the future of the Indonesian nation. There are several programs and stages that have been implemented. Such as education and outreach about stunting and how to prevent it, education about health and hygiene, and providing additional food

Machine learning-based prediction of breast cancer growth rate in-vivo

BackgroundDetermining the rate of breast cancer (BC) growth in vivo, which can predict prognosis, has remained elusive despite its relevance for treatment, screening recommendations and medicolegal practice. We developed a model that predicts the rate of in vivo tumour growth using a unique study cohort of BC patients who had two serial mammograms wherein the tumour, visible in the diagnostic mammogram, was missed in the first screen.MethodsA serial mammography-derived in vivo growth rate (SM-INVIGOR) index was developed using tumour volumes from two serial mammograms and time interval between measurements. We then developed a machine learning-based surrogate model called Surr-INVIGOR using routinely assessed biomarkers to predict in vivo rate of tumour growth and extend the utility of this approach to a larger patient population. Surr-INVIGOR was validated using an independent cohort.ResultsSM-INVIGOR stratified discovery cohort patients into fast-growing versus slow-growing tumour subgroups, wherein patients with fast-growing tumours experienced poorer BC-specific survival. Our clinically relevant Surr-INVIGOR stratified tumours in the discovery cohort and was concordant with SM-INVIGOR. In the validation cohort, Surr-INVIGOR uncovered significant survival differences between patients with fast-growing and slow-growing tumours.ConclusionOur Surr-INVIGOR model predicts in vivo BC growth rate during the pre-diagnostic stage and offers several useful applications

The multifaceted roles of ER and Golgi in metabolic cardiomyopathy

Metabolic cardiomyopathy is a significant global financial and health challenge; however, pathophysiological mechanisms governing this entity remain poorly understood. Among the main features of metabolic cardiomyopathy, the changes to cellular lipid metabolism have been studied and targeted for the discovery of novel treatment strategies obtaining contrasting results. The endoplasmic reticulum (ER) and Golgi apparatus (GA) carry out protein modification, sorting, and secretion activities that are more commonly studied from the perspective of protein quality control; however, they also drive the maintenance of lipid homeostasis. In response to metabolic stress, ER and GA regulate the expression of genes involved in cardiac lipid biogenesis and participate in lipid droplet formation and degradation. Due to the varied roles these organelles play, this review will focus on recapitulating the alterations and crosstalk between ER, GA, and lipid metabolism in cardiac metabolic syndrome

Mechanisms and therapeutic prospects of diabetic cardiomyopathy through the inflammatory response

The incidence of heart failure (HF) continues to increase rapidly in patients with diabetes. It is marked by myocardial remodeling, including fibrosis, hypertrophy, and cell death, leading to diastolic dysfunction with or without systolic dysfunction. Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in the absence of coronary artery disease. DCM is partially induced by chronic systemic inflammation, underpinned by a hostile environment due to hyperglycemia, hyperlipidemia, hyperinsulinemia, and insulin resistance. The detrimental role of leukocytes, cytokines, and chemokines is evident in the diabetic heart, yet the precise role of inflammation as a cause or consequence of DCM remains incompletely understood. Here, we provide a concise review of the inflammatory signaling mechanisms contributing to the clinical complications of diabetes-associated HF. Overall, the impact of inflammation on the onset and development of DCM suggests the potential benefits of targeting inflammatory cascades to prevent DCM. This review is tailored to outline the known effects of the current anti-diabetic drugs, anti-inflammatory therapies, and natural compounds on inflammation, which mitigate HF progression in diabetic populations

Multi-organ FGF21-FGFR1 signaling in metabolic health and disease

Metabolic syndrome is a chronic systemic disease that is particularly manifested by obesity, diabetes, and hypertension, affecting multiple organs. The increasing prevalence of metabolic syndrome poses a threat to public health due to its complications, such as liver dysfunction and cardiovascular disease. Impaired adipose tissue plasticity is another factor contributing to metabolic syndrome. Emerging evidence demonstrates that fibroblast growth factors (FGFs) are critical players in organ crosstalk via binding to specific FGF receptors (FGFRs) and their co-receptors. FGFRs activation modulates intracellular responses in various cell types under metabolic stress. FGF21, in particular is considered as the key regulator for mediating systemic metabolic effects by binding to receptors FGFR1, FGFR3, and FGFR4. The complex of FGFR1 and beta Klotho (β-KL) facilitates endocrine and paracrine communication networks that physiologically regulate global metabolism. This review will discuss FGF21-mediated FGFR1/β-KL signaling pathways in the liver, adipose, and cardiovascular systems, as well as how this signaling is involved in the interplay of these organs during the metabolic syndrome. Furthermore, the clinical implications and therapeutic strategies for preventing metabolic syndrome and its complications by targeting FGFR1/β-KL are also discussed