•Of the 27 studies included, there were 26 instruments used to measure ACEs.•Comparison between studies was challenging due to different methodology approaches.•Many studies lacked explanations for ...using specific reliability and validity tests.•Standardization in ACE measurement is needed to improve ACE prevalence estimations.
The study objectives were to 1) examine what methodological approaches have been used to determine adverse childhood experiences (ACE) prevalence and 2) determine the prevalence of different ACEs.
A scoping review was conducted on 2009–2020 articles focused on persons 17 years and younger, highlighting screening and surveillance of ACEs, and evaluating the psychometrics of ACE screening tools.
A descriptive analysis categorized results of 27 articles into key methodological themes (i.e., study design, self vs. caregiver reporting, location/setting). Majority of the studies were cross-sectional (81.5%), self-reporting (74.1%) and focused on neglect, bullying/victimization and violence. There were 26 unique instruments used to assess ACEs. The prevalence for ACEs reported in the literature varied widely based on factors such as the type of ACEs examined, instrument, self vs. caregiver reporting, age group, and setting.
Synthesis of our findings highlights the need for standardization in ACE measurement as they contribute to variations in ACE prevalence estimations and understanding the overall burden ACEs have on a population. Recommendations for improving ACE measurement among U.S. children and adolescents were provided.
Anastomosis of catheterising channels (Mitrofanoff and ACE) to the skin can be a challenge. The Kelly VV plasty is a straightforward solution but has been described only as a point of technique.
We ...used the previously described method with minor modification.
The technique has been used in 14 patients, including 9 children and 5 adults for Mitrofanoff,ACE and Monti channels.
At a median follow-up of 25 months all patients continue to catheterise; none have required revision surgery.
The Kelly VV plasty is a potentially robust solution to the problem of skin anastomosis; technique merits wider adoption and evaluation.
Serum angiotensin-converting enzyme (ACE) is the only biomarker routinely used in the laboratory diagnostics of sarcoidosis, and ACE inhibitor (ACEi) drugs are among the most prescribed drugs ...worldwide. Taking ACEi can mislead medical teams by lowering ACE activity, delaying diagnosis and giving a false impression of disease activity of sarcoidosis. We aimed to develop a simple method to detect the presence of ACEi drugs in samples, to investigate the ACEi medication-caused interference and consequences in a retrospective study.
ACE activity and the level of ACE inhibition were determined for 1823 patients with suspected sarcoidosis. These values were compared with the therapeutic information at the first and follow-up visits.
A total of 302 patients had biochemical evidence of an ACEi drug effect during diagnostic ACE activity testing. In their case, ACE activity was significantly lower (median(IQR): 4.41 U/L(2.93-6.72)) than in patients not taking ACEi (11.32 U/L(8.79-13.92), p<0.01). In 62 sarcoidosis patients, the ACEi reduced ACE activity to the reference range or below. Only in 40 % of the cases was the medication list recorded in the outpatient chart and only in 3 cases was low ACE activity associated with ACEi use. 67 % of the repeated ACE activity measurements were also performed during ACEi therapy.
Our study revealed that the use of ACEi is common in patients with suspected sarcoidosis. The ACE activity lowering effect of ACEi drugs may escape the attention of medical teams which can lead to diagnostic errors and unnecessary tests. Nevertheless, these pitfalls can be avoided by using a method suggested by our team.
Angiotensin converting enzyme (ACE) is not only a critical component in the renin-angiotensin system (RAS), but also suggested as an important mediator for immune response and activity, such as ...immune cell mobilization, metabolism, biogenesis of immunoregulatory molecules, etc. The chronic duration of cardiovascular diseases (CVD) has been increasingly considered to be triggered by uncontrolled pathologic immune reactions from myeloid cells and lymphocytes. Considering the potential anti-inflammatory effect of the traditional antihypertensive ACE inhibitor (ACEi), we attempt to elucidate whether ACE and its catalytically relevant substances as well as signaling pathways play a role in the immunity-related pathogenesis of common CVD, such as arterial hypertension, atherosclerosis and arrythmias. ACEi was also reported to benefit the prognoses of COVID-19-positive patients with CVD, and COVID-19 disease with preexisting CVD or subsequent cardiovascular damage is featured by a significant influx of immune cells and proinflammatory molecules, suggesting that ACE may also participate in COVID-19 induced cardiovascular injury, because COVID-19 disease basically triggers an overactive pathologic immune response. Hopefully, the ACE inhibition and manipulation of those associated bioactive signals could supplement the current medicinal management of various CVD and bring greater benefit to patients' cardiovascular health.
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•Increased ACE expression in immune cells proactively enhances immune reactions such as anti-infection and anti-tumor activity, probably via its catalytic products, metabolism reprogramming of immune cells or intracellular signaling pathways regulation.•ACE participates in the pathogenesis of various chronic CVD not only through blood pressure mediation, but also through immunomodulation.•ACE inhibitor ameliorating CVD relies on both the antihypertensive and anti-inflammatory effects.
Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in ...the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin1-7. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin1-7 also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the ‘adverse’ ACE→Angiotensin II→AT1 receptor axis and the ‘protective’ ACE2→Angiotensin1-7→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin1-7. In this setting, recombinant ACE2, angiotensin1-7 and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.
•Angiotensin-converting enzyme (ACE) modulates a variety of bioactive peptides in the renin–angiotensin system and endogenous opioid system.•There is an emerging interest in the utilization of ACE ...inhibitors for pain management.•Treatment with ACE inhibitors is beneficial in neuropathy, cancer and migraine-associated pain.•Targeting ACE could enable engagement of the body’s own mechanism for pain modulation.
The renin–angiotensin system (RAS) is known to affect diverse physiological processes that affect the functioning of many key organs. Angiotensin-converting enzyme (ACE) modulates a variety of bioactive peptides associated with pain. ACE inhibitors (ACEis) have found applications in the treatment of cardiovascular, kidney, neurological and metabolic disorders. However, ACEis also tend to display undesirable effects, resulting in increased pain sensitization and mechanical allodynia. In this review, we provide comprehensive discussion of preclinical and clinical studies involving the evaluation of various clinically approved ACEis. With the emerging knowledge of additional factors involved in RAS signaling and the indistinct pharmacological role of ACE substrates in pain, extensive studies are still required to elucidate the mechanistic role of ACE in pain perception.
Diabetic stress acts on the cardiac tissue to induce cardiac hypertrophy and fibrosis. Diabetes induced activated renin angiotensin system (RAS) has been reported to play a critical role in mediating ...cardiac hypertrophy and fibrosis. Angiotensin converting enzyme (ACE) in producing Angiotensin-II, promotes cardiomyocyte hypertrophy and fibrotic damage. ACE2, a recently discovered molecule structurally homologous to ACE, has been reported to be beneficial in reducing the effect of RAS driven pathologies.
In vivo diabetic mouse model was used and co-labelling immunostaining assay have been performed to analyse the fibrotic remodeling and involvement of associated target signaling molecules in mouse heart tissue. For in vitro analyses, qPCR and western blot experiments were performed in different groups for RNA and protein expression analyses.
Fibrosis markers were observed to be upregulated in the diabetic mouse heart tissue as well as in high glucose treated fibroblast and cardiomyocyte cells. Hyperglycemia induced overexpression of YAP1 leads to increased expression of β-catenin (CTNNB1) and ACE with downregulated ACE2 expression. The differential expression of ACE/ACE2 promotes TGFB1-SMAD2/3 pathway in the hyperglycemic cardiomyocyte and fibroblast resulting in increased cardiac fibrotic remodeling.
In the following study, we have reported YAP1 modulates the RAS signaling pathway by inducing ACE and inhibiting ACE2 activity to augment cardiomyocyte hypertrophy and fibrosis in hyperglycemic condition. Furthermore, we have shown that hyperglycemia induced dysregulation of ACE-ACE2 activity by YAP1 promotes cardiac fibrosis through β-catenin/TGFB1 dependent pathway.
•Diabetes stress in cardiac tissue results in alteration in cellular architecture and promotes cardiac fibrotic remodeling.•Hyperglycemia activates YAP1 and β-catenin activity leading to cardiac fibrosis through TGF-β/SMAD2/3 pathway.•Hyperglycemia induced dysregulation of ACE-ACE2 activity by YAP/β-catenin signaling promotes cardiac fibrotic remodeling.•ACE2 proves to be a key protective molecule in ameliorating hyperglycemic stress induced fibrotic remodeling in adult heart.
Early kidney failure in the hereditary type IV collagen disease, Alport syndrome, can be delayed by renin-angiotensin inhibitors. However, whether all patients and all different genotypes respond ...equally well to this kidney-protective therapy remains unclear. Here, we performed a retrospective study on 430 patients with male X-linked Alport syndrome to examine the relationships among kidney prognosis, genotype, and treatment effect in a large cohort of Japanese patients. We analyzed the clinical features, genotype-phenotype correlation, and kidney survival period for patients treated with or without renin-angiotensin inhibitors. As a result, the median kidney survival period of patients in this cohort was found to be at 35 years with a strong genotype-phenotype correlation. The median age at the onset of end stage kidney disease (ESKD) significantly differed between patients treated with and without renin-angiotensin inhibitors (over 50 years versus 28 years, respectively). Moreover, these drugs delayed the onset of ESKD in patients with truncating variants for 12 years, extending the median age from 16 years to 28 years. Thus, our results confirmed a strong genotype-phenotype correlation in patients with male X-linked Alport syndrome. Additionally, it was suggested that renin-angiotensin inhibitors could significantly delay ESKD progression. Despite these therapies, patients with truncating variants developed ESKD at the median age of 28 years.
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The purpose of this research is to create a robust predictive load frequency control (RPLFC) for power systems with unpredictable parameters and temporal delays in communication networks. The study ...looks closely at the communication of delay constraints across the various control regions as well as the relationship between delay restrictions and control gains. In addition, the usage of delay restrictions as a new performance index to steer controller design is discussed, along with the regulation of the controller for a trade-off between delay tolerance and dynamic reaction, and opting for the upper bound of the sampling period of a discrete realization of the controller, and the upper bound of the fault counter of the communication channel. All of these topics are brought up in the context of determining how to steer controller design. To determine whether or not the proposed technique is useful, simulation studies have all been outfitted with PID-type controllers and have been run for both single-area and three-area LFC schemes. MATLAB/SIMULINK served as the platform upon which the simulations were carried out.
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