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Purpose: To investigate the clinical effectiveness of beta-blockers (BBs) and renin-angiotensin-aldosterone system (RAAS) inhibitors in chronic heart failure with preserved ejection fraction (HFpEF). Methods: 100 patients with HFpEF admitted to The Third Affiliated Hospital of Qiqihar Medical University, China, between April and June 2023 were stratified into five groups. Beta-blocker (BB) group received bisoprolol, angiotensin-converting enzyme inhibitor (ACEI) group received benazepril hydrochloride, angiotensin II receptor blocker (ARB) group received candesartan, angiotensin receptor neprilysin inhibitor (ARNI) group received sacubitril valsartan, and mineralocorticoid receptor antagonist (MRA) group received spironolactone. Differences in clinical effectiveness, six-minute walking distance (6MWD), cardiac functionality, quality of life, and survival rate were compared among the groups. Results: Beta-blocker group showed the highest efficacy. After treatment, all groups except MRA showed significant improvement in 6MWD. Also, ACEI, ARB, and ARNI groups exhibited significantly longer 6 MWD than MRA group (p < 0.05). Left ventricular ejection fraction levels showed significant improvement in the ACEI, ARNI, and MRA groups (p < 0.05), while pulmonary artery pressure (PAP) decreased in the BB, ACEI, ARNI, and MRA groups (p < 0.05). After treatment, the Minnesota Living with Heart Failure Questionnaire (MLHFQ) scores of BB, ACEI, ARB, and ARNI groups were significantly lower than before treatment (p < 0.05). All five groups significantly exhibited decline in NTproBNP levels after treatment (p < 0.05). However, at 18-month follow-up, there was no significant difference in survival rates among the groups (p > 0.05). Conclusion: Beta-blockers (BBs) and RAAS inhibitors show promising activity in HFpEF, bisoprolol enhances cardiac function, benazepril improves symptoms, candesartan aids exercise and sacubitril valsartan elevates cardiac class. However, none of these drugs significantly improves clinical outcomes. [ABSTRACT FROM AUTHOR]

Background. IgA nephropathy (IgAN) is currently the most common primary glomerular disease, accounting for approximately 36.7% to 58.2% of primary glomerular disease in kidney biopsies in China. Definitive diagnosis depends on immunopathological examination of the kidney. The prognosis of this disease was generally considered to be good, but recent studies have found that about half of patients can progress to end-stage renal disease within 30 years of onset. Because the pathogenesis is unknown, there is no specific treatment. Objective. To evaluate the efficacy and safety of glycosides of Tripterygium wilfordii (GTW) in combination with renin-angiotensin system (RAS) inhibitors for the treatment of IgAN. Methods. Search Embase, Pubmed, Cochrane, CNKI, Web of Science, Wanfang, and VIP for all randomized controlled trials (RCTs) on treating IgAN with RASI from the self-built database to December 2021. Relevant data were searched and collected separately by two reviewers. The Cochrane risk of bias model was used for quality assessment, and RevMan 5.3 was used for data analysis. Results. Thirteen Chinese publications with a total of 958 patients were finally included. There was no statistically significant difference in baseline information (including laboratory data and clinical parameters) between the two groups of patients. The urine protein quantification in both groups showed a significant decreasing trend as the treatment duration increased. At 3, 6, 9, and 12 months after treatment, urine protein was significantly lower than the baseline value in both the observation and control groups (P < 0.05). During the follow-up period, there was no statistical difference in blood creatinine (Scr) and eGFR values between the two groups compared with the baseline values (P > 0.05). Patients with CKD stage 2 achieved a higher remission rate compared with patients with CKD stage 3, with a statistically significant difference (P < 0.05), and the difference between the two groups was not significant for patients in the same stage. There was no statistically significant difference in the total effective rate between the two groups (P > 0.05). During the follow-up period, there was no statistically significant difference in urine protein quantification, Scr, and eGFR between the two groups. In terms of the incidence of adverse reactions, the observation group was less than the control group, and there was a significant difference between the two groups (P < 0.05). Conclusion. GTW combined with RASI is one of the safe and effective treatment modes for IgAN nephropathy. It can not only effectively reduce the excretion of urinary protein in patients and delay the progression of chronic kidney disease but also has less serious side effects and is well tolerated by patients, so it can be a new choice of therapeutic drugs for this group of patients. [ABSTRACT FROM AUTHOR]

Infection with SARS-CoV-2, the causative agent of the COVID-19 pandemic, originated in China and quickly spread across the globe. Despite tremendous economic and healthcare devastation, research on this virus has contributed to a better understanding of numerous molecular pathways, including those involving γ-aminobutyric acid (GABA), that will positively impact medical science, including neuropsychiatry, in the post-pandemic era. SARS-CoV-2 primarily enters the host cells through the renin–angiotensin system's component named angiotensin-converting enzyme-2 (ACE-2). Among its many functions, this protein upregulates GABA, protecting not only the central nervous system but also the endothelia, the pancreas, and the gut microbiota. SARS-CoV-2 binding to ACE-2 usurps the neuronal and non-neuronal GABAergic systems, contributing to the high comorbidity of neuropsychiatric illness with gut dysbiosis and endothelial and metabolic dysfunctions. In this perspective article, we take a closer look at the pathology emerging from the viral hijacking of non-neuronal GABA and summarize potential interventions for restoring these systems. [ABSTRACT FROM AUTHOR]

Background: Coronavirus disease 2019 (COVID‐19) is an emerging, rapidly evolving pandemic, hypertension is one of the most common co‐existing chronic conditions and a risk factor for mortality. Nearly one‐third of the adult population is hypertensive worldwide, it is urgent to identify the factors that determine the clinical course and outcomes of COVID‐19 patients with hypertension. Methods and results: 148 COVID‐19 patients with pre‐existing hypertension with clarified outcomes (discharge or deceased) from a national cohort in China were included in this study, of whom 103 were discharged and 45 died in hospital. Multivariate regression showed higher odds of in‐hospital death associated with high‐sensitivity cardiac troponin (hs‐cTn) > 28 pg/ml (hazard ratio [HR]: 3.27, 95% confidence interval [CI]: 1.55–6.91) and interleukin‐6 (IL‐6) > 7 pg/ml (HR: 3.63, 95% CI:1.54–8.55) at admission. Patients with uncontrolled blood pressure (BP) (n = 52) which were defined as systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg for more than once (≥2 times) during hospitalization, were more likely to have ICU admission (p = 0.037), invasive mechanical ventilation (p = 0.028), and renal injury (p = 0.005). A stricter BP control with the threshold of 130/80 mm Hg was associated with lower mortality. Treatment with renin‐angiotensin‐aldosterone system (RAAS) suppressors, including angiotensin‐converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), and spironolactone, was associated with a lower rate of ICU admission compared to other types of anti‐hypertensive medications (8 (22.9%) vs. 25 (43.1%), p = 0.048). Conclusion: Among COVID‐19 patients with pre‐existing hypertension, elevated hs‐cTn and IL‐6 could help clinicians to identify patients with fatal outcomes at an early stage, blood pressure control is associated with better clinical outcomes, and RAAS suppressors do not increase mortality and may decrease the need for ICU admission. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome corona virus 2 hit strongly and hardly the entire globe for more than 1 year with a morbidity exceeding 139 million and a mortality approaching 3 million worldwide since its emergence in China in December 2019 until April 2021. Although being termed after its ancestor the acute respiratory syndrome corona virus that emerged in 2002. Yet, the current corona virus has its unique devastating presentations being pulmonary and extra pulmonary. In the current review, a highlight on the role played by corona virus 2 on pathogenesis and outcome of stroke is presented with an attempt to point to the most approved ways through which the corona virus induce stroke being disturbance in renin angiotensin system and angiotensin-converting enzyme 2 receptors downregulation, endothelial cell damage with coagulopathy, cytokine storm, and platelet as well as outcome and risks in patients who are suffering stroke with modifiable vascular risk factors and catching the severe acute respiratory syndrome corona virus 2. [ABSTRACT FROM AUTHOR]

The outbreak of a newly identified coronavirus, the SARS-CoV-2 (alternative name 2019-nCoV), capable of jumping across species causing zoonosis with severe acute respiratory syndromes (SARS), has alerted authorities worldwide. Soon after the epidemic was first detected in the city of Wuhan in the Hubei Province of China, starting in late December 2019, the virus spread over multiple countries in different continents, being declared a pandemic by March 2020. The demographic characteristics of the infected patients suggest that age, sex, and comorbidities are predictive factors for the fatality of the infection. The mechanisms of viral entry into the human host cells seem to be in a close relationship with the mechanisms of regulating the renin-angiotensin system (RAS), which may explain the pathogenesis associated with the infection. This brings new insights into the possibilities of exploiting viral entry mechanisms to limit associated complications by means of enhancing the resistance of the infected patients using methods of regulating the RAS and strategies of modulating ACE2 expression. In this perspective article we exploit the mechanisms of COVID-19 pathogenesis based on the demographic characteristics of the infected patients reported in the recent literature and explore several approaches of limiting the initial steps of viral entry and pathogenesis based on viral interactions with ACE2 and RAS. We further discuss the implications of reproductive hormones in the regulation of the RAS and investigate the premise of using endocrine therapy against COVID-19. [ABSTRACT FROM AUTHOR]

Salvia miltiorrhiza Bge. (Labiatae) (SMB) is applied clinically for management of diabetic osteoporosis in China, and research results has suggested its potential action on renin–angiotensin system (RAS). This study screens and explores naturally occurring bioactive constituents from the root of SMB acting on renin activity and evaluates its osteoprotective efficacy in diabetic mice. Human embryonic kidney (HEK) 293 cells, engineered to express human renin, were used as an in vitro model to identify bioactive compound, tanshinone IIA, inhibiting renin activity. The C57BL/6 mice (n = 10 in each group) with diabetes induced by streptozotocin (STZ) were intraperitoneally injected with tanshinone IIA (10 and 30 mg/kg). The mice without STZ treatment and the diabetic mice treated with aliskiren were used as non-diabetic control and positive control, respectively. Tanshinone IIA was found to display inhibitory effects on renin activity of HEK-293 cells; moreover, it down-regulated protein expression of ANG II in human renin-expressed HEK-293 cells. Treatment of diabetic mice with tanshinone IIA with both doses could significantly decrease ANG II level in serum (from 16.56 ± 1.70 to 10.86 ± 0.68 and 9.14 ± 1.31 pg/mL) and reduce ANG II expression in bone, consequently improving trabecular bone mineral density and micro-structure of proximal tibial end and increasing trabecular bone area of distal femoral end in diabetic mice. This study revealed beneficial effects of tanshinone IIA on bone of diabetic mice, and potentially suggested the application of Salvia miltiorrhiza in the treatment of osteoporosis and drug development of tanshinone IIA as a renin inhibitor. [ABSTRACT FROM AUTHOR]

Since the first cases of atypical pneumonia linked to the Huanan Seafood Wholesale Market in Wuhan, China, were described in late December 2019, the global landscape has changed radically. In March 2020, the World Health Organization declared COVID-19 a global pandemic, and at the time of writing this review, just over three million individuals have been infected with more than 200,000 deaths globally. Numerous countries are in 'lockdown', social distancing is the new norm, even the most advanced healthcare systems are under pressure, and a global economic recession seems inevitable. A novel coronavirus (SARS-CoV-2) was identified as the aetiological agent. From experience with previous coronavirus epidemics, namely the severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) in 2004 and 2012 respectively, it was postulated that the angiotensin-converting enzyme-2 (ACE2) receptor is a possible port of cell entry. ACE2 is part of the renin-angiotensin system and is also associated with lung and cardiovascular disorders and inflammation. Recent studies have confirmed that ACE2 is the port of entry for SARS-CoV-2. Male sex, advanced age and a number of associated comorbidities have been identified as risk factors for infection with COVID-19. Many high-risk COVID-19 patients with comorbidities are on ACE inhibitors and angiotensin receptor blockers, and this has sparked debate about whether to continue these treatment regimes. Attention has also shifted to ACE2 being a target for future therapies or vaccines against COVID-19. In this review, we discuss COVID-19 and its complex relationship with ACE2. [ABSTRACT FROM AUTHOR]

The outbreak of a newly identified coronavirus, the SARS-CoV-2 (alternative name 2019-nCoV), capable of jumping across species causing zoonosis with severe acute respiratory syndromes (SARS), has alerted authorities worldwide. Soon after the epidemic was first detected in the city of Wuhan in the Hubei Province of China, starting in late December 2019, the virus spread over multiple countries in different continents, being declared a pandemic by March 2020. The demographic characteristics of the infected patients suggest that age, sex, and comorbidities are predictive factors for the fatality of the infection. The mechanisms of viral entry into the human host cells seem to be in a close relationship with the mechanisms of regulating the renin-angiotensin system (RAS), which may explain the pathogenesis associated with the infection. This brings new insights into the possibilities of exploiting viral entry mechanisms to limit associated complications by means of enhancing the resistance of the infected patients using methods of regulating the RAS and strategies of modulating ACE2 expression. In this perspective article we exploit the mechanisms of COVID-19 pathogenesis based on the demographic characteristics of the infected patients reported in the recent literature and explore several approaches of limiting the initial steps of viral entry and pathogenesis based on viral interactions with ACE2 and RAS. We further discuss the implications of reproductive hormones in the regulation of the RAS and investigate the premise of using endocrine therapy against COVID-19. [ABSTRACT FROM AUTHOR]

The emergency of SARS-CoV-2 in China started a novel challenge to the scientific community. As the virus turns pandemic, scientists try to map the cellular mechanisms and pathways of SARS-CoV-2 related to the pathogenesis of Coronavirus Disease 2019 (Covid-19). After transmembrane angiotensin-converting enzyme 2 (ACE2) has been found to be SARS-CoV-2 receptor, we hypothesized an immune-hematological mechanism for Covid-19 based on renin-angiotensin system (RAS) imbalance to explain clinical, laboratory and imaging findings on disease course. We believe that exaggerated activation of ACE/Angiotensin II (Ang II)/Angiotensin Type 1 (AT1) receptor RAS axis in line with reduction of ACE2/Angiotensin-(1-7)/Mas receptor may exert a pivotal role in the pathogenesis of Covid-19. In this perspective, we discuss potential mechanisms and evidence on this hypothesis. [ABSTRACT FROM AUTHOR]

A case study of 36 Chronic heart failure (CHF) patients is presented. It is mentioned that in China CHF is a leading cause of death. The article discusses the benefits of forest bathing such as therapeutic effect on patients with hypertension and chronic obstructive pulmonary disease. It notes that forest bathing can lead to the decline in endothelin-1 (ET-1) and inhibits the activities of renin which are the major causes of the progression of CHF.

This study was conducted to explore whether the renin C-5312T, angiotensin II type 1 receptor A1166C, and angiotensin-converting enzyme I/D polymorphisms were associated with ambulatory blood pressure (BP) and central hemodynamics in an untreated hypertensive population. A total of 471 participants with no previous treatment for raised BP were eligible for the study. Ambulatory and central BP were measured. DD carriers had the highest daytime systolic/diastolic BP, nighttime systolic BP, 24-hour systolic BP, and 24-hour diastolic BP values, whereas carriers of DD had higher central systolic BP and augmentation index compared with those with the II genotype. Multivariate regression analysis demonstrated that DD genotype was independently associated with 24-hour systolic BP, 24-hour diastolic BP, central systolic BP, and central augmentation index. There was an independent association of the angiotensin-converting enzyme polymorphism with central and ambulatory BP in Chinese patients with hypertension. [ABSTRACT FROM AUTHOR]

Summary: The local renin-angiotensin system (RAS) is closely related to bone metabolism. However, it is unknown whether the local RAS is related to bone mineral density (BMD) in glucocorticoid-induced osteoporosis (GIOP). Here, we revealed that the two main characteristics of GIOP might inhibit bone formation and enhance bone resorption. Introduction: The aim of this study is to assess the expression of the main RAS components in the trabecular bone of lumbar vertebrae in GIOP and analyze the relationship between the major RAS components and BMD. Methods: We collected 96 inpatient cases of lumbar disc herniation from patients who underwent dual-energy X-ray absorptiometry examinations followed by surgical treatment in our hospital. Patients were divided into the GIOP group ( n = 48) and control group ( n = 48). The circulating and local expression levels of the main RAS components were examined. The correlation between the main RAS components and BMD was then analyzed. Results: The mRNA expression of local bone angiotensin type 1 and 2 receptors (AT1R and AT2R, respectively) and RANKL was higher in the GIOP group compared with the control group ( p < 0.001), but there was no difference in the circulating protein levels between groups ( p > 0.05). Multiple logistic regression analysis revealed that AT1R and AT2R expression and the RANKL/OPG ratio in local bone were negatively associated with BMD ( p < 0.001, odds ratio (OR) 1.236, 95 % confidence interval (CI) 1.207-1.333; p < 0.001, OR 1.971, 95 % CI 1.809-2.233; and p < 0.001, OR 1.676, 95 % CI 1.546-1.845, respectively). Conclusion: This study provides evidence that the role of local RAS is related to BMD in GIOP patients, and suggests that local RAS might influence RANKL/OPG signaling to modulate bone metabolism. [ABSTRACT FROM AUTHOR]

Gene polymorphisms of the renin–angiotensin system are involved in the pathophysiology of hypertension. We genotyped 4 polymorphisms of angiotensinogen (AGT) gene A-20C (rs5050), A-6G (rs5051), C3889T (rs4762), and C4072T (rs699) by polymerase chain reaction-restriction fragment length polymorphism in 652 patients and 780 controls to examine the association of AGT and hypertension in a Northern Han Chinese population. There were significant differences in the distribution of genotypes and allele frequencies at C4072T between the patients and the controls (both P < .01); patients with CC genotype had a higher risk of hypertension (odds ratio = 1.7, 95% confidence interval 1.4–2.1). The distribution of genotypes at A-6G was significantly different between patients and controls (P < .05). No other significant differences in genotypes or frequencies were observed. No association was observed between the haplotypes of AGT and hypertension. The AGT-6A and 4072C alleles are associated with susceptibility to hypertension in this population. [ABSTRACT FROM PUBLISHER]

Background: Aliskiren is the first oral direct renin inhibitor to be approved for the treatment of hypertension. The pharmacokinetic and pharmacodynamic profile of aliskiren has been extensively characterized in Caucasian individuals; however, drug disposition, treatment response and tolerability can vary among ethnic groups, and these variations are difficult to predict. Objective: To evaluate the single- and multiple-dose pharmacokinetics of aliskiren in healthy Chinese subjects. Methods: This was a randomized, single-blind, parallel-group, placebocontrolled study. On day -1, subjects were randomized to one of four cohorts (aliskiren 75, 150, 300 or 600 mg). On day 1, eight individuals in each cohort received a single dose of active treatment and two received placebo. Subjects randomized to aliskiren 300 mg received additional once-daily doses on days 5-11 to establish steady-state pharmacokinetics. Subjects receiving aliskiren 75, 150 or 600mg (cohorts 1, 2 and 4) completed the study at the end of the 96-hour pharmacokinetic assessment period. Subjects receiving aliskiren 300mg (cohort 3) had additional pharmacokinetic assessments on days 5-15. The study was carried out at the Peking Union Medical College Hospital, Beijing, China, and included 40 healthy Chinese subjects. The main outcome measures were the pharmacokinetic parameters for aliskiren, including area under the plasma concentration-time curve from time zero to infinity (AUC∞) and maximum plasma concentration (Cmax). Results: Aliskiren AUC∞ and Cmax increased greater than proportionally across the 8-fold dose range (75-600 mg; mean AUC∞ 291-4726 ng · h/mL, mean Cmax 62-699 ng/mL), but a dose-proportional 2-fold increase was observed within the clinically approved dose range (150-300 mg; mean AUC∞ 876-1507 ng ∞ h/mL, mean Cmax 137-271 ng/mL). At steady state, the mean AUC during the dosage interval (AUC∞) for aliskiren 300mg (1532 ± 592 ng · h/mL)was similar to theAUC∞ observed following a single dose. Conclusion: Aliskiren exhibits similar single-dose and steady-state pharmacokinetics in Chinese subjects compared with those observed in Caucasian individuals in previous studies. [ABSTRACT FROM AUTHOR]

Lagopsis supina (Steph. ex Willd.) lk. -Gal. ex Knorr. has been used as a diuretic agent in China for centuries with limited scientific evidence. This study investigated the diuretic efficacy and underlying mechanism of a macroporous adsorption resin with 30% ethanol elution fraction from L. supina (LSC) in saline-loaded rats and to identify its phytochemicals by ultra-high-performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (UHPLC-qTOF-MS/MS). As a result, 18 phenylpropanoids, 14 flavonoids and 15 others were identified in LSC, among which stachysoside A and acteoside could be the main bio-active constituents responsible for the diuretic effect. In parallel, the daily administration of LSC (16, 32 and 64 mg/kg) markedly promoted urinary excretion after 2 h of treatment. Moreover, LSC had no effect on urinary Na+ and K+ concentrations, as well as on serum Na+-K+-ATPase activity. Meanwhile, LSC significantly decreased the serum levels of angiotensin II (Ang II), anti-diuretic hormone (ADH), aldosterone (ALD), aquaporin (AQP) 1, AQP2 and AQP3, suppressed renal AQP1, AQP2, and AQP3 mRNA expressions, down-regulated AQP1, AQP2 and AQP3 protein levels, and up-regulated serum atriopeptin (ANP) level in a dose-dependent manner. These findings suggest that LSC has acute and prolonged diuretic effects by inhibiting the AQPs, RAAS, and upregulation of atriopeptin in saline-loaded rats, and this finding support LSC as a novel diuretic agent. [Display omitted] • LSC possess prominent diuretic effect in saline-loaded rats. • LSC inhibits the AQPs and RAAS, as well as promotes atriopeptin. • Stachysoside A and acteoside are two main bio-active constituents in LSC. [ABSTRACT FROM AUTHOR]

Background. Cross-sectional studies investigated the impact of renin-angiotensin system (RAS) gene polymorphism on left ventricular mass index (LVMI) with conflicting results. We conducted a longitudinal study to investigate the influence of the angiotensin-converting enzyme (ACE) insertion/deletion (l/D) and angiotensinogen (AGT) M235T and angiotensin 11 type 1 receptor (ATI R) A1166C gene polymorphisms on the LVMI and geometry. Methods. Of 1500 people screened, 110 nondiabetic normotensive elderly Chinese persons were recruited and received echocardiography at baseline and at the 2nd and 4th year follow-up. No participants had a history of organic heart disease or chronic medication. The gene polymorphisms were analyzed by using polymerase chain reaction. Results. Participant age was 71.9 ± 3.9 years (range 60-81 years). The prevalence of concentric remodeling, eccentric hypertrophy, and concentric hypertrophy was significantly increased as well as LVMI after 4 years (all p < .05). These changes and the magnitude of LVMI increase were significantly higher in participants carrying the ACE D allele than non-D-allele carriers (all p < .05). This association was still significant in multivariate analyses (p < .02). A similar analysis showed a borderline significance in the ATI R but not in the AGT gene polymorphism. Conclusions. This longitudinal study showed that the aging process was associated with an increase of LVMI and changes of geometry. The RAS gene polymorphism, especially the ACE D allele, might modulale these changes in the Chinese population. This provides further knowledge that is essential in the assessment of cardiac disease and the determination of the left ventricular structure in older persons. [ABSTRACT FROM AUTHOR]

• SARS-CoV-2 urged at end of 2019 as the causative of (COVID-19) causing a worldwide dissemination of the disease. • Its pathophysiology is complex with the involvement of a diversity of systems and can evolve to death. • Among the various systems involved in the disease, the renin-angiotensin (RAS) and kallikrein-kinin (KKS) systems stand out. • Here we described RAS and KKS in COVID-19 suggesting their importance in the evolution of the disease. • Some possibilities for drug repositioning in treating COVID-19 is also discussed. In November 2019 the first cases of a novel acute respiratory syndrome has been reported in Wuhan province, China. Soon after, in January 2020 the World Health Organization declared a pandemic state due to the dissemination of a virus named SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the cause of coronavirus disease 2019 (COVID-19). Being an unknown disease, it is essential to assess not only its main characteristic features and overall clinical symptomatology but also its patient infection mode and propagation to design appropriate clinical interventions and treatments. In this review the pathophysiology of SARS-CoV-2 infection and how the virus enters the cells and activates the immune system are described. The role of three systems involved in the SARS- CoV-2 infection (renin-angiotensin, kinin and coagulation systems) is discussed with the objectives to identify and try to explain several of the events observed during the evolution of the disease and to suggest possible targets for therapeutic interventions. [ABSTRACT FROM AUTHOR]

The first cases of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2 or COVID-19) infections were recorded in China in November 2019. Since its appearance in China at the end of last year, the virus has spread to all continents causing a "global pandemic". To date, some aspects remain to be investigate about the pathophysiology of this viral infection. One of the aspects to be still clarified is the correlation between the renin-angiotensin system (RAS) and SARS-CoV-2 infection. RAS is a physiological system playing a key role in different human body functions regulation. SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE-2), a component of RAS, as a potential factor of cell penetration and infectivity; in addition, in the different infection stages, a functional variation of the RAS has been noted. In this article, we discuss the correlation between the role of RAS and system-modifying agents, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs) and direct renin inhibitors (DRIs), with SARS-CoV-2 infection. [ABSTRACT FROM AUTHOR]

Background: Hand, foot and mouth disease (HFMD) remains a burdensome health issue in mainland China. Enterovirus71 (EV-A71) is the main pathogen of severe HFMD. Continuous hemofiltration improves fluid overload, restores kidney function and alleviates inflammatory reactions. The aim of the present study was to evaluate the effects of continuous veno-venous hemodiafiltration (CVVHDF) on severe HFMD caused by EV-A71(EV-A71-HFMD) in a pediatric intensive care unit (PICU).Methods: A retrospective observational study was performed in a tertiary university PICU from January 2012 to December 2016. Children with severe EV-A71-HFMD complicated by cardiopulmonary failure were included. The patients were divided into a CVVHDF group and a conventional therapy (control) group (non-CVVHDF). The demographics, characteristics, and outcomes between the groups were collected and analyzed.Results: Twenty-nine patients with severe EV-A71-HFMD were enrolled. The 28-day mortality was 17.6% (3/17) in the CVVHDF group and 33.3% (4/12) in the non-CVVHDF group, with no statistical significance between the two groups (P = 0.403). The median interval between CVVHDF initiation and PICU admission was 6 (4,8.5) hrs, and the median duration of CVVHDF was 48 (36, 64) hrs. The left ventricular ejection fraction (LVEF) and cardiac index (CI) in the CVVHDF group were improved after treatment. The plasma levels of catecholamines and renin-angiotensin-aldosterone system (RAAS) substances in the CVVHDF group were significantly decreased after treatment. The decreased catecholamines and RAAS substances included adrenalin (169.8 [145.5, 244.6] vs. 148.0 [109.0, 208.1] ng/L, P = 0.033), dopamine (152.7 [97.0, 191.1] vs. 96.0 [68.0, 160.9] ng/L, P = 0.026), angiotensin II (185.9 [125.2, 800.0] vs. 106.0 [90.8, 232.5] ng/L, P = 0.047), aldosterone (165.7 [94.0, 353.3] vs. 103.3 [84.3, 144.3] ng/L, P = 0.033), and renin (1.12 [0.74, 3.45] vs. 0.79 [0.52, 1.25] μg/L/h, P = 0.029), CONCLUSIONS: CVVHDF reduced the levels of catecholamines and RAAS substances and improved cardiovascular function. Continuous hemodiafiltration may represent a potential therapy in patients with severe EV-A71-HFMD complicated with cardiopulmonary failure. [ABSTRACT FROM AUTHOR]

Background: The angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been suggested to influence susceptibility to essential hypertension (EH), but the results of many individual studies are conflicting. Aim and methods: To explore the relationship between the ACE gene I/D polymorphism and EH in the Chinese population, 67 separated studies were analyzed in a meta-analysis including 21 058 participants. The electronic databases PubMed, Embase, Web of Science, China Biological Medicine Database and China National Knowledge Infrastructure were searched. The pooled odds ratio (ORs) and its corresponding 95% confidence interval were calculated by the random effects model. Results: In this ACE I/D gene polymorphism meta-analysis, the distribution of the D allele frequency was 0.45 for the EH group and 0.40 for the control group. The summary OR for the distribution frequency of D allele was 1.27 (5% confidence interval 1.17-1.37). The heterogeneity among the 67 studies was also significant ( P < 0.00001, I2= 71.4%). There was a significant association between distribution frequency of the D allele and EH risk in Han, Kazakh, Tibetan, Zhuang and unclassified nationalities ( P < 0.05). In contrast, in the national minorities, such as Mongolian, Uigur, Yi, Dongxiang, Yugu, Korean and Gamel, the association between distribution frequency of the D allele and EH risk was not significant ( P > 0.05). Conclusions: In the whole Chinese population, the D allele was significantly linked with EH susceptibility. However, the relation between the I/D polymorphism and EH is still inconclusive in some national minorities and must await larger scale studies. [ABSTRACT FROM AUTHOR]