Purpose: The recent outbreak of coronavirus disease 2019 (COVID-19) is the worst global crisis after the Second World War. Since no successful treatment and vaccine have been reported, efforts to enhance the knowledge, attitudes, and practice of the public, especially the high-risk groups, are critical to manage COVID-19 pandemic. Thus, this study aimed to assess knowledge, attitude, and practice towards COVID-19 among patients with chronic disease. Patients and Methods: A cross-sectional study was conducted among 404 chronic disease patients from March 02 to April 10, 2020, at Addis Zemen Hospital, Northwest Ethiopia. Both bivariable and multivariable logistic regression analyses with a 95% confidence interval were fitted to identify factors associated with poor knowledge and practice towards COVID-19. The adjusted odds ratio (AOR) was used to determine the magnitude of the association between the outcome and independent variables. P-value < 0.05 was considered statistically significant. Results: The mean age of the participants was 56.5± 13.5. The prevalence of poor knowledge and poor practice was 33.9% and 47.3%, respectively. Forty-one percent of the participants perceived that avoiding of attending a crowded population is very difficult. Age (AOR=1.05, (95% CI (1.01– 1.08)), educational status of “can’t read and write” (AOR=7.1, 95% CI (1.58– 31.93)), rural residence (AOR=19.0, 95% CI (6.87– 52.66)) and monthly income (AOR=0.8, 95% CI (0.79– 0.89)) were significantly associated with poor knowledge. Being unmarried (AOR=3.9, 95% CI (1.47– 10.58)), cannot read and write (AOR=2.7, 95% CI (1.03– 7.29)), can read and write (AOR=3.5, 95% CI (1.48– 8.38)), rural residence (AOR=2.7, 95% CI (1.09– 6.70)), income of < 7252 Ethiopian birr (AOR=2.3, 95% CI (1.20– 4.15)) and poor knowledge (AOR=8.6, 95% CI (3.81– 19.45)) were significantly associated with poor practice. Conclusion: The prevalence of poor knowledge and poor practice was high. Leaflets prepared in local languages should be administered and health professionals should provide detailed information about COVID-19 to their patients.

Ghrelin is a relatively novel multifaceted hormone that has been found to exert a plethora of physiological effects. In this review, we found/confirmed that ghrelin has effect on all body systems. It induces appetite; promotes the use of carbohydrates as a source of fuel while sparing fat; inhibits lipid oxidation and promotes lipogenesis; stimulates the gastric acid secretion and motility; improves cardiac performance; decreases blood pressure; and protects the kidneys, heart, and brain. Ghrelin is important for learning, memory, cognition, reward, sleep, taste sensation, olfaction, and sniffing. It has sympatholytic, analgesic, antimicrobial, antifibrotic, and osteogenic effects. Moreover, ghrelin makes the skeletal muscle more excitable and stimulates its regeneration following injury; delays puberty; promotes fetal lung development; decreases thyroid hormone and testosterone; stimulates release of growth hormone, prolactin, glucagon, adrenocorticotropic hormone, cortisol, vasopressin, and oxytocin; inhibits insulin release; and promotes wound healing. Ghrelin protects the body by different mechanisms including inhibition of unwanted inflammation and induction of autophagy. Having a clear understanding of the ghrelin effect in each system has therapeutic implications. Future studies are necessary to elucidate the molecular mechanisms of ghrelin actions as well as its application as a GHSR agonist to treat most common diseases in each system without any paradoxical outcomes on the other systems.

Caspase-1 is the first and extensively studied inflammatory caspase that is activated through inflammasome assembly. Inflammasome is a cytosolic formation of multiprotein complex that aimed to start inflammatory response against infections or cellular damages. The process leads to an auto-activation of caspase-1 and consequent maturation of caspase-1 target molecules such as interleukin (IL)-1β and IL-18. Recently, the role of caspase-1 and inflammasome in inflammatory-induced noncommunicable diseases (NCDs) like obesity, diabetes mellitus (DM), cardiovascular diseases (CVDs), cancers and chronic respiratory diseases have widely studied. However, their reports are distinct and even they have reported contrasting role of caspase-1 in the development and progression of NCDs. A few studies have reported that caspase-1/inflammasome assembley has a protective role in the initiation and progression of these diseases through the activation of the noncanonical caspase-1 target substrates like gasdermin-D and regulation of immune cells. Conversely, others have revealed that caspase-1 has a direct/indirect effect in the development and progression of several NCDs. Therefore, in this review, we systematically summarized the role of caspase-1 in the development and progression of NCDs, especially in obesity, DM, CVDs and cancers.

Mitochondria are organelles with highly dynamic ultrastructure maintained by flexible fusion and fission rates governed by Guanosine Triphosphatases (GTPases) dependent proteins. Balanced control of mitochondrial quality control is crucial for maintaining cellular energy and metabolic homeostasis; however, dysfunction of the dynamics of fusion and fission causes loss of integrity and functions with the accumulation of damaged mitochondria and mitochondrial deoxyribose nucleic acid (mtDNA) that can halt energy production and induce oxidative stress. Mitochondrial derived reactive oxygen species (ROS) can mediate redox signaling or, in excess, causing activation of inflammatory proteins and further exacerbate mitochondrial deterioration and oxidative stress. ROS have a deleterious effect on many cellular components, including lipids, proteins, both nuclear and mtDNA and cell membrane lipids producing the net result of the accumulation of damage associated molecular pattern (DAMPs) capable of activating pathogen recognition receptors (PRRs) on the surface and in the cytoplasm of immune cells. Chronic inflammation due to oxidative damage is thought to trigger numerous chronic diseases including cardiac, liver and kidney disorders, neurodegenerative diseases (Parkinson’s disease and Alzheimer’s disease), cardiovascular diseases/atherosclerosis, obesity, insulin resistance, and type 2 diabetes mellitus.

Objective: This study aimed to assess the level of aspartate aminotransaminase (AST), alanine aminotransaminase (ALT) and gamma-glutamyltransferase (GGT), and their association with type 2 diabetes mellitus in Northwest Ethiopia. Results: Using a cross-sectional study, blood samples were collected from 192 Type 2 diabetes mellitus (T2DM) participants and 192 healthy age and sex-matched volunteers. The study was carried out from May to August 2017. The serum concentration of aspartate aminotransaminase, alanine aminotransaminase, and gamma-glutamyltransferase were measured using A25 Bio-system fully automatic chemistry analyzer and using the manufacturer’s kit of the machine. Liver function test results of T2DM participant were significantly higher than those of the control group, serum ALT (46.06 ± 22. 38 IU/L) and serum AST (42.94 ± 19. 08 IU/L), P < 0.001, while the level of GGT in both study groups was not significantly associated (P = 0.065). In conclusion, the evaluation of liver marker enzymes showed a significant association with Type 2 diabetes participants compared with the controls.

In response to obesity-associated chronic inflammatory disorders, adipose tissue releases a biologically active peptide known as leptin. Leptin activates the secretion of chemical mediators, which contribute to the pathogenesis of chronic inflammatory disorders, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and psoriasis. Conversely, adiposity and obesity are the major aggravating risk factors in the pathogenesis of metabolic syndrome (MetS), including type II diabetes mellitus and obesity-associated hypertension. Elevated level of leptin in obesity-associated hypertension causes an increase in the production of aldosterone, which also results in elevation of arterial blood pressure. Hyperleptinemia is associated with the progress of the atherosclerosis through secretion of pro-inflammatory cytokines, like interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), IL-17, and other cytokines to promote inflammation. The release of those cytokines leads to chronic inflammatory disorders and obesity-associated MetS. Thus, the aberrant leptin level in both MetS and chronic inflammatory disorders also leads to the complication of cardiovascular diseases (CVD). Therapeutic target of leptin regarding its pro-inflammatory effect and dysregulated sympathetic nervous system activity may prevent further cardiovascular complication. This review mainly assesses the mechanism of leptin on the pathogenesis and further cardiovascular risk complication of chronic inflammatory disorders.