Higher Uric Acid Concentrations Research Articles

Prognostic Value of Right Ventricular Dysfunction in Patients With Decompensated Chronic Heart Failure

Aim To determine the incidence rate and the practical significance of right ventricular dysfunction (RVD) in the development of cardiovascular complications in patients with decompensated chronic heart failure (DCHF).Material and methods This prospective, single-site observational study included 171 patients older than 18 years with NYHA functional class (FC) II-IV chronic heart failure (CHF) who were hospitalized for DCHF. Standard and extended 2D and 3D echocardiography (EchoCG) was performed for all patients on admission. Additionally, functional characteristics of the right ventricle (RV) were evaluated in the 3D mode followed by autonomic 3D processing with a EchoPac station (USA). RVD was taken as a disorder of two or more RV functional parameters according to results of 2D EchoCG, or a reduced RV free wall strain according to results of 2D speckle-tracking EchoCG, or a reduced RV ejection fraction (EF) according to results of 3D EchoCG. Statistical analysis was performed with a SPSS Statistics v. 26.0 software.Results The incidence rate of RVD in general population of patients with DCHF was 75.4 % (n=129). A higher prevalence of RVD was observed in patients with CHF with a low left ventricular (LV) EF (90.1 %). Patients with RVD had a more severe clinical status (significantly higher FC and higher Clinical Condition Scale (CCS) scores), more frequent atrial fibrillation (AF), and higher concentrations of uric acid and total bilirubin. RVD significantly correlated with male sex (odds ratio (OR), 2.05; 95 % confidence interval (CI), 1.01–4.19; р=0.046) and AF (OR, 3.52; 95 % CI, 1.71–7.26; р<0.001). Patients with RVD had lower values of both LV and RV function. Lower LV EF and AF increased the probability of RVD by 1.06 times (95 % CI, 0.90–0.98; р=0.001) and by 2.63 times (95 % CI, 1.08–6.40; р=0.001), respectively. Evaluation of the predictive significance of RV parameters measured by 2D and 3D EchoCG showed only effects of RV EF (2D) and RV global longitudinal strain (GLS) (3D) on all-cause hospitalization. RVD as evaluated by accepted criteria did not influence adverse outcomes.Conclusion The determined incidence, correlations, and the predictive value of RVD in patients with DCHF indicated the appropriateness of assessing the RV function to optimize the management of patients regardless of the CHF phenotype.

The Inter-Trimester Variation and Prognostic Value of Creatinine, Cystatin C and Uric Acid in Preeclamptic Patients: A Retrospective Study

Background: This study aimed to evaluate the clinical significance of maternal serum creatinine, cystatin C, and uric acid levels in relation to fetal death in pregnant women with preeclampsia. Methods: This retrospective study evaluated 708 women with preeclampsia, and 738 healthy pregnant women were selected as control. Medical records were reviewed to collect obstetric, neonatal, and biochemical data, including creatinine, cystatin C, and uric acid concentrations. Results: Maternal serum creatinine, cystatin C, and uric acid concentrations were significantly higher in the preeclamptic group than in the control (p < 0.05). Preeclamptic women in the fetal death group had significantly higher creatinine levels during their second and third trimesters, and higher uric acid concentrations throughout the pregnancy compared to the fetal survival group. Preeclamptic patients were divided into four groups based on quartiles of uric acid levels. The overall fetal survival rate in patients with upper-quartile uric acid concentrations was significantly lower than those with low uric acid levels during pregnancy. Multivariate logistic regression analysis revealed that uric acid concentration was a significant risk factor for fetal death in the first and second trimesters in the preeclamptic group (p < 0.05). Conclusions: In pregnant women with preeclampsia, fetal death was associated with upper-quartile uric acid concentrations in the first and second trimesters. Uric acid levels can be an indicator of fetal death in the early and middle stage of pregnancy.

A Limited Effect of Chronic Renal Insufficiency on the Colon Microbiome.

A Limited Effect of Chronic Renal Insufficiency on the Colon Microbiome.

Enzyme-free and wide-range portable colorimetric sensing system for uric acid and hydrogen peroxide based on copper nanoparticles

Uric acid (UA) is the final product of purine metabolism. A high concentration of UA in body fluid may lead to kidney stones, gout, and some cardiovascular diseases. Therefore, the non-invasive daily monitoring of UA is of great significance for both hyperuricemia patients and fit people. However, most of the current detection methods for UA are enzyme-dependent which limits the application scenarios and lacks portable instruments for on-site detection, including optics and electrochemistry. In this work, an enzyme-free and wide-range colorimetric sensor for UA and H2O2 detection was developed based on a mercaptosuccinic acid (MSA)-modified Cu nanoparticles (CuNPs). Under the action of UA or H2O2, with the cleavage of MSAs on the CuNPs surface, small Cu particles are further aggregated into larger particles with a lightning violet color. With the employment of the multi-channel handheld automatic photometer (MHAP), the concentration of UA and H2O2 can be determined on-site according to the absorbance measurement by the photodiodes. The linear range of UA was 5 μM-4.5 mM with the limit of detection (LOD) of 3.7 μM, while the linear range of H2O2 was 5 mM–500 mM and 5 μM-5 mM with the LOD of 4.3 μM. This approach has been applied to the detection of UA in human urine, providing more possibilities for non-invasive home health monitoring, community medical diagnosis, and broader prospects of on-site disease detection.

Critical Hypermagnesemia in Preeclamptic Women Undera MagnesiumSulfate Regimen: Incidence and Associated Risk Factors.

Magnesium sulfate is used as prophylaxis and treatment of severe preeclampsia/eclampsia, albeit its safety and toxicity are a concern. We designed this study to estimate the incidence of critical hypermagnesemia in severely preeclamptic women undera magnesiumsulfate regimen at 8h following its administration and to identify the associated risk factors as the primary outcomes. Also, secondary outcomes were to compare baseline characteristics, laboratory findings, and maternal-neonatal complications stratified by the baseline serum magnesium (Mg2+) in those women, and to assess the degree of agreement between patellar reflex and serum Mg2+ concentration 8h following magnesiumsulfate administration. We conducted a retrospective study including severely preeclamptic women receiving magnesium sulfate from June 2016 to May 2021. We enrolled 429 women in the study. Two-hundred sixty-one (60.8%) of the included women developed critical hypermagnesemia. Preeclamptic women with high baseline serum Mg2+ concentration demonstrated significantly affected renal functions, hepatic transaminase activities, and low platelet count as well as more reported maternal complications compared to those with low baseline serum Mg2. Multivariable logistic regression revealed that a lower gestational age, a higher uric acid concentration, and a higher baseline serum Mg2+ concentration were independently associated with an increased risk of critical hypermagnesemia. The agreement between deep tendon reflex assessment and serum Mg2+ concentration was slight although not significant. The maternal-neonatal outcomes were non-significant in women with critical hypermagnesemia. More vigilant monitoring through assessment of both serum Mg2+ concentration and deep tendon reflex should be considered especially in high-risk women.

Association between metabolic syndrome and uric acid: a systematic review and meta-analysis

This systematic review and meta-analysis aim to provide the best evidence on the association between metabolic syndrome (MetS) and uric acid (UA) by determining the size of the effect of this biomarker on MetS. The review protocol is registered with PROSPERO (CRD42021231124). The search covered the PubMed and Scopus databases. Methodological quality was assessed with the STROBE tool, overall risk of bias with RevMan (Cochrane Collaboration) and quality of evidence with Grade Pro. Initially, 1582 articles were identified. Then, after excluding duplicates and reviewing titles and abstracts, 1529 articles were excluded from applying the eligibility criteria. We included 43 papers (56 groups) comparing UA concentrations between subjects 91,845 with MetS and 259,931 controls. Subjects with MetS had a higher mean UA of 0.57 mg/dl (95% CI 0.54–0.61) (p < 0.00001). Given the heterogeneity of the included studies, the researchers decided to perform subgroups analysis. Men with MetS have a higher UA concentration mg/dl 0.53 (95% CI 0.45–0.62, p < 0.00001) and women with MetS 0.57 (95% CI 0.48–0.66, p < 0.00001) compared to subjects without MetS. Assessment of UA concentration could provide a new avenue for early diagnosis of MetS, as a new biomarker and the possibility of new therapeutic targets.

A geniposide-phospholipid complex ameliorates posthyperuricemia chronic kidney disease induced by inflammatory reactions and oxidative stress

Hyperuricemia is a common metabolic disease and is one of the factors that could induce chronic kidney disease (CKD). Geniposide (GEN) is a typical natural iridoid glucoside compound with a series of biological activities, but the poor bioavailability of GEN limits its clinical application. In this context, the pharmacological activity of the geniposide-phospholipid complex (GEN-PLC) in ameliorating posthyperuricemia CKD was evaluated by in vitro and in vivo experiments in this study. In vitro cell experiments showed that GEN-PLC treatment markedly decreased inflammatory cytokine levels and reactive oxygen species levels compared with those of GEN in uric acid-treated HKC cells. In vivo research results confirmed that a high concentration of uric acid could cause CKD by increasing inflammatory cytokines and reactive oxygen species in hyperuricemic mice. At the same time, GEN-PLC could regulate the PI3K/AKT/NF-κB and Keap1/Nrf2/HO-1 signaling pathways to effectively inhibit the inflammatory response and oxidative stress, thereby ameliorating posthyperuricemia CKD, and the therapeutic effect was better than that of GEN. In addition, the preparation technology of GEN-PLC was optimized, and the physiochemical analysis explained the intermolecular interactions of the two components. Based on the research results, GEN-PLC could enhance the bioavailability of GEN and become a promising candidate for clinical drug development.

PB2053: PRIMARY ARTERIAL HYPERTENSION IN MYELOPROLIFERATIVE NEOPLASMS: A SYSTEMATIC REVIEW

Background: Patients diagnosed with myeloproliferative neoplasms (MPNs) are prone to experience thrombotic events and often experience a high burden of cardiovascular comorbidities. Primary arterial hypertension (HTN) remains one of the most common comorbidities in the elderly. However, the impact of HTN on MPNs is unclear. Aims: Report on the occurrence of HTN in MPNs. Describe its epidemiology, influence on development of thrombosis, HTN treatment strategies. Methods: Systematic search in PubMed/Medline, Web of Science and SCOPUS, from the inception of these databases to retrieve relevant English-written articles. Eligibility criteria: 1. Confirmed MPNs diagnosis, 2. Confirmed HTN diagnosis, 3. Studies reported on the epidemiology of HTN in MPNs, impact of HTN on the development of thrombosis or on the therapeutic options used to treat HTN in MPNs. We excluded studies investigating secondary HTN, e.g., drug-induced HTN. Results: The systematic search resulted in 590 potentially relevant manuscripts. After removal of duplicates and screening of abstracts/titles (n=503), 87 manuscripts were selected for full-text review. After applying the eligibility criteria and full-text evaluation, 25 articles were excluded and the remaining 62 were entered into the qualitative/quantitative analysis. HTN emerged as the most common comorbidity in MPNs, affecting 41-63% of primary myelofibrosis (PMF), 40-64% of essential thrombocythemia (ET), 46-90% of polycythemia vera (PV) cases. In PV, the presence of HTN was associated with decreased serum free epinephrine and aldosterone levels, reduced retinal microperfusion, elevated kidney arteries resistance, JAK2-V617F mutation and high-risk PV. In PMF, it was linked with high uric acid concentrations and elevated risk of thrombosis (OR=1.96). PV subjects with HTN were non-dippers, suffered from systolic/diastolic dysfunction as assessed by cardiac ultrasound, displayed elevated cell-free hemoglobin and nitrite/nitrate ratio, and an increased risk of thrombosis (HR=1.77). HTN in ET was associated with overall thrombosis, especially arterial thrombosis (HR=1.91-3.8). The cardio-IPSET score was superior in predicting thrombosis in ET patients with HTN. Individuals with MPNs and HTN exhibited signs of carotid artery injury, end-organ damage, increased albumin-to-creatinine ratio, P-selectin concentrations and were prone to develop kidney dysfunction. Moreover, stroke was more common in MPNs with concomitant HTN (HR=4.24) and HTN was a predictor of ischemic stroke recurrence in MPNs. The risk of thrombosis in MPNs was higher if HTN was also associated with other cardiovascular risk factors, i.e., dyslipidemia, diabetes or smoking. The risk of cerebral venous sinus thrombosis was lower in MPNs with co-occurring HTN. In terms of treatment options for patients with HTN and MPNs, angiotensin-converting enzyme inhibitors (ACEI), e.g., lisinopril, and calcium-channel blockers (CCB - nifedipine for hypertensive emergencies) have been successfully used. The recommendation to avoid the use of diuretics in patients with elevated blood viscosity, e.g., PV, remains unaltered. Summary/Conclusion: Our findings suggest that HTN is the most common comorbidity in MPNs and is associated with development of thrombosis, end-organ damage, i.e., retinal and kidney dysfunction. Integration of HTN in the current scores employed to predict the development of thrombosis and stratify MPNs subjects in warranted. Screening for HTN in MPNs is urgently needed. Accurate management strategies based on the use ACEI and CCB need further exploration in MPNs with associated HTN.

The potential influence of high uric acid exposure on surface and corrosion susceptibility of pure titanium

This study investigated the corrosion susceptibility of pure titanium under uric acid exposure for 7 days based on surface analysis. The prepared pure titanium specimens, exposed to different concentrations of uric acid, were examined for surface microstructure, surface element composition and surface wettability using scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS) and static contact angle measurement, respectively. The corrosion behaviors of titanium specimens were measured by open-circuit potential (OCP), electrochemical impedance spectroscopy (EIS) and potentiodynamic polarization. The titanium ion release from the prepared specimens, which were immersed in Hank’s balanced salt solution (HBSS) containing different amount of uric acid, was measured by inductively coupled plasma atomic emission spectrometry (ICP-AES). More irregular pitting holes were observed on titanium surfaces exposed to a high concentration of uric acid, and XPS analyses revealed that the amount of titanium dioxide (TiO2) decreased. Titanium surfaces pre-treated with high uric acid became more hydrophobic. Furthermore, the results of OCP and potentiodynamic polarization tests showed increased corrosion susceptibility of titanium samples, while EIS data indicated more active corrosion behavior of titanium materials. The high concentration of uric acid also induced titanium ion release. High concentration of uric acid negatively influenced the surface characteristics and corrosion properties of titanium materials, which destroyed the titanium oxide film barrier. High uric acid exposure increased corrosion susceptibility of pure titanium specimens and accelerated titanium ion release.Graphical abstract

Lycopodium clavatum as a homeopathic treatment in Magellanic penguins (Sphenicus magellanicus)

Background: Uric acid is the main form of excretion of nitrogenous components in birds. The assessment verification samples, control, check of uric acid concentrations is widely used to detect kidney disease. High concentrations (up to five times) of uric acid in plasma can lead to the precipitation of this acid in the form of crystals, which accumulate in the tissues, mainly in the synovial joints and the viscera surface. Aims: report the evolution of homeopathic treatment in increased uric acid in Magellanic penguins (Spheniscus magellanicus) from Santo André Municipal Zoo. Methodology: 12 animals showed an increase in uric acid (reference values 0,3-16,1mg/dL) and received homeopathic treatment with Lycopodium clavatum 6cH. The protocol established was the administration of two globules of Lycopodium clavatum 6cH, once a day, inside fishes offered in the animal's beak. Treatment started on 25/09/2019. On 30/10/2019 was collected a new blood sample, those who were not discharged were kept on treatment and new collections were made on 27/11/2019 and 17/12/2019. Results: 8 animals had an average uric acid of 20.45mg /dl and responded to the 35-days treatment, normalizing the biochemical values ​​with an average of 12.24mg /dl. Two animals with 18.27 mg /dl were discharged in 62 days with 11.70 mg /dl and another two penguins with 19.85 mg /dl were discharged in 82 days later with 9.57 mg /dl of uric acid. Conclusion: Homeopathy proved to be successful in the treatment of increased uric acid in Magellanic penguins, easy to administer, affordable and without side effects.

Inflammasomes in placental explants of women with preeclampsia cultured with monosodium urate may be modulated by vitamin D

ABSTRACT Objectives Preeclampsia (PE) is an important syndrome of gestation characterized by placental and systemic inflammation. High plasma concentration of uric acid are frequently associated with inflammation and endothelial dysfunction and may contribute to PE pathogenesis. This study aimed to evaluate the vitamin D (VD) immunomodulatory effect on the NLRP1/NLRP3 inflammasomes in placental explants from preeclamptic (PE) and normotensive (NT) pregnant women. Study design Placental explants from 10 late-onset PE (LOPE), 10 early-onset PE (EOPE), and 10 NT pregnant women were cultured with or without monosodium urate (MSU) and VD. Main outcome measures Gene and protein expression of NLRP1, NLRP3, HMGB1, caspase-1, interleukin-1 beta (IL-1β), and IL-18 were determined by quantitative PCR and Western blotting/ELISA. Statistical significance was accepted at p < 0.05. Results Basal gene and protein expression of NLRP1/NLRP3 and IL-1β, IL-18 and HMGB1 were significantly higher in explants from EOPE compared to LOPE and NT pregnant women. In addition, culture with MSU increased these inflammatory markers, and concomitant treatment with MSU+VD decreased this effect. Conclusions The results demonstrated that NLRP1 and NLRP3 inflammasomes are upregulated in the placental tissue of EOPE women, associated with high production of inflammatory cytokines. The in vitro treatment with VD downregulated placental inflammasomes induced by MSU, suggesting its immunomodulatory role in the systemic inflammation of PE.

Uric acid, as a double-edged sword, affects the activity of epidermal growth factor (EGF) on human umbilical vein endothelial cells by regulating aging process

ABSTRACT Uric acid (UA) is the main metabolite of the human body. Although UA is only a product of metabolism, it is important biological regulator. Epidermal growth factor (EGF) has important biological functions. However, so far, the effect of UA on EGF’s activity has not been revealed. For this, in the current study, we systematically studied the effect of OA on the biological activity of EGF. Human Umbilical Vein Endothelial Cells (HUVECs) were used as an in vitro model, and Western-blot, RT-PCR, laser scanning confocal microscopy (CLSM) and co-localization analyses were carried out. The results showed that high concentration of UA (10 mg/dl) severely affected the biological activity of EGF. High concentration of UA suppressed the activity of EGF, and inhibited the biological effect of EGF on the HUVECs. However, it is interesting that EGF-mediated intracellular signaling was significantly down-regulated in the H2O2-induced senescent HUVEC, and physiological concentration of UA could at least partially restore the EGF-mediated signaling. Further work showed that physiological concentration of UA (5 mg/dl) shows the anti-aging effect. Taken together, current research indicates that UA may be a ‘double-edged sword’, physiological concentration of UA may be beneficial, but high concentrations of uric acid (UA) are harmful.

Abstract WP237: Uric Acid Expressed Within Carotid Atherosclerotic Plaque And Serum Uric Acid Are Associated With Cerebrovascular Events

Introduction: Uric acid (UA) level within carotid plaque specimens and its association with cerebrovascular events has not been detected or quantified. Systemically, serum uric acid (SUA) is a marker of inflammation and risk factor for atherosclerosis. However, its association with carotid plaque instability and subsequent cerebrovascular events remains unclear. Hypothesis: We hypothesized that UA may play a role in carotid artery atherosclerosis and stroke pathogenesis. In patients undergoing carotid endarterectomy (CEA), we aimed to determine whether UA is present differentially in carotid plaques of symptomatic versus asymptomatic patients and whether SUA is associated with cerebrovascular symptoms before surgery and major adverse cardiovascular events (MACE) in the follow-up to CEA. Methods: We prospectively collected 32 carotid plaques during CEA. We qualitatively assessed the presence of UA by using Gomori methenamine silver (GMS) staining and immunohistochemistry with anti-UA antibodies. We extracted and measured the quantity of UA in carotid plaques by using an enzymatic colorimetric assay. A retrospective analysis of a clinical database of 534 consecutive patients who underwent CEA was performed. We defined as symptomatic those patients with history of stroke, TIA and amaurosis fugax. Results: UA positive staining was detected in higher number of carotid plaques from symptomatic compared to asymptomatic patients on both staining, GMS [20 (86.9%) vs 2 (22.2%); p=0.001] and immunohistochemistry anti-UA [16 (69.5%) vs 1 (11.1%); p=0.004]. Moreover, we found a significantly higher concentration of UA in carotid plaque from symptomatic compared to asymptomatic patients [25.1 (9.5) μg/g vs 17.9 (3.8) μg/g; p=0.021]. SUA level in patients prior to CEA was significantly higher in the symptomatic compared to the asymptomatic group [6.0 (4.8-7.1) mg/dL vs 5.2 (4.4-6.3) mg/dL; p&lt;0.001] and it was significantly higher in patients who developed MACE after CEA versus those that did not [6.0 (4.8-7.1) mg/dL vs 5.4 (4.5-6.6) mg/dL; p=0.021]. Conclusions: UA may provide a mechanistic explanation as systemic biomarker and potential tissue contributor for carotid plaque instability and subsequent cerebrovascular and cardiovascular symptoms.

Evidence for the effect of soluble uric acid in augmenting endoplasmic reticulum stress markers in human peripheral blood mononuclear cells.

There is evidence regarding the association of hyperuricemia with inflammatory disorders. Hence, it has been of particular interest to dissect the exact role of alteration in uric acid (UA) levels in the context of inflammation. Recently, the endoplasmic reticulum (ER) stress pathway has come into the forefront as a possible mechanism linking hyperuricemia to inflammation. Here, we intended to examine the role of UA in the presence or absence of a second stimulus, LPS, in human peripheral blood mononuclear cells (PBMCs), and analyzed ROS production as well as expression of ER stress markers: GRP78 and CHOP, and inflammatory cytokines.PBMCs were isolated using Ficoll gradient centrifugation from healthy volunteers. Cell viability was measured by MTT assay. PBMCs were treated with an increasing concentration of soluble UA (0, 5, 12, and 20mg/dl) for 20h, followed by the addition of 100ng/mL of LPS or vehicle for another 4h. Real time-PCR was performed to investigate the mRNA expression of GRP78, CHOP, TNF-α, IL-1β, and IL-6, and western blot was used to investigate the protein levels of GRP78 and CHOP. Moreover, ELISA was used to evaluate the protein levels of TNF-α, IL-1β, and IL-6. Finally, intracellular ROS production was determined using fluorescent probes (DCFH-DA).High concentrations of UA either alone or combined with LPS increased the protein levels of GRP78 and CHOP. On the other hand, LPS alone increased the protein levels of GRP78 and CHOP. However, there was no significant difference between the mRNA expression of GRP78, CHOP, TNF-α, IL-1β, and IL-6 when PBMCs were treated with UA. High concentrations of UA augmented LPS-stimulated IL-1β transcript and protein levels as well as TNF-α protein levels in PBMC culture. Moreover, high concentrations of UA along with LPS significantly increased intracellular ROS production.It seems that a high concentration of UA not only induces the protein levels of ER stress markers in PBMCs but also augments the impact of LPS on the levels of pro-inflammatory markers and ROS production.

Uric acid: The role in the pathophysiology and the prediction in the diagnosis of Parkinson's disease: A Turkish-based study.

Oxidative stress has been associated as an essential contributor to the development of neurodegenerative diseases. Recent developments in the field of Parkinson's Disease (PD) pathophysiology have led to a renewed interest in this field. As an antioxidant, uric acid (UA) has arisen as a potential neuroprotectant. Higher concentrations of UA are linked to reducing the risk of the development of the disease and preventing its progression. However, the expositions are unsatisfactory because the outcomes of these reports have not been consistent. This study is set out to assess the association of whether lower UA concentrations increased the PD risk by investigating its relationship with patients' demographic and clinical data, and to determine whether previous studies are compatible with the Turkish-sampled population. Furthermore, we aimed to determine UA's probability of being an early-stage diagnostic marker. A total of 305 patients and 100 healthy controls were included. Serum UA levels of patients and controls were compared with clinical features. We classified the patients into three motor subtypes and determined the disease severity by modified Hoehn&Yahr Staging Scale (mH&Y) and Unified Parkinson's Disease Rating Scale (UPDRS). Standardized Mini-Mental State Examination (MMSE-TR) was assessed for cognition. There were not any significant differences of age and sex between patients and controls (p=0.030, p=0.132). The mean UA was 5.06±1.33 mg/dL in patients and 5.46±1.44 in controls, and a statistical significance was detected (p=0.022). The mean MMSE-TR were 24.83±4.35 in patients and 27.09±2.13 in controls, and statictical significance was revealed (p=0.001). The mean duration of the disease was 6.31±4.16 years, mean UPDRS scores were 59.74±22.33, and mH&Y scores were 2.29±0.91. In binary comparisons, patients with tremor-dominant motor subtype had lower UA concentrations than controls (p=0.014). ROC curve analysis revealed UA's cut-off as ≤9.15, the specificity was 99.3, the sensitivity was 10.0, and the area under the curve was 0.576 (p<0.005). Regression analysis revealed age as an independent risk factor on UA values. Oxidative stress might be a factor in the development of PD, and UA may be a possible prospective protecting factor in the clinical course of the disease. However, it does not affect the severity. Our results support that lower uric acid concentrations are associated with PD; however, it is not a powerful indicator for predicting PD risk. As we reveal more about UA and its effect in further investigations, its significant role will become well-defined.

Facile one-pot method of AuNPs/PEDOT/CNT composites for simultaneous detection of dopamine with a high concentration of ascorbic acid and uric acid.

In this research, a facile one-pot method was used to synthesize gold/poly-3,4-ethylene-dioxythiophene/carbon nanotube (AuNPs/PEDOT/CNTs) composite material. The composite material was investigated by Fourier Transform Infrared spectroscopy (FTIR), X-ray diffraction (XRD) and Scanning Electron Microscopy (SEM). Then the synthesized nanocomposite material was dropped on a bare glassy carbon electrode (GCE) to improve the detection performance of dopamine with a high concentration of ascorbic acid and uric acid. The electrochemical behavior of AuNPs/PEDOT/CNTs/GCE was studied by Cyclic Voltammetry (CV), Differential Pulse Voltammetry (DPV) and electrochemical impedance spectroscopy (EIS). Under optimum conditions, AuNPs/PEDOT/CNTs/GCE showed a good linear response in the concentration range from 9.14 to 29.704 μM with a detection limit (LOD) and sensitivity of 0.283 μM and 1.557 μA μM−1, respectively. This sensor was applied to detect practical samples with good average recovery. It also exhibited good reproducibility and stability.

A Successful Management of Hyperuricaemia Through Ayurveda Medications: A Case Series

Uric acid is a heterolytic compound of Carbon, Nitrogen, Oxygen and Hydrogen which is produced by the metabolism breakdown of purine nucleotides. Elevated level of uric acid in blood is called hyperuricemia. This condition arises due to over production or under secretion of uric acid. High blood concentration of uric acid can lead to Gout and are associated with other medical conditions. In Ayurveda science Vaatarkta disease is described which having similarities to the conditions of hyperuricemia, So hyperuricaemia can be corelated with Vaatarakta as Ayurveda perspective. In this case series, three cases of Hyperuricaemia were treated with Navakarshika ghana vati - 250 mg x2 TID after meal for one month with Kashyam and Amrutadi tailam-10ml OD with 100ml lukewarm water or milk on empty stomach for one month, gets very effective & quick response in hyperuricaemia. Both are pacified and normalised the level of uric acid. Also didn’t found any adverse drug reaction of both medicines.

Correlation between Serum Uric Acid with Type 2 Diabetes Mellitus and its Complications

Type 2 diabetes mellitus is becoming more common over the world, making it a major health concern. Many research has been carried a link among both higher uric acid concentrations in the body and a higher incidence of type 2 diabetes mellitus. On a biochemical level, uric acid has been proved to have a negative impact on insulin sensitivity in animals. When nitric oxide, essential for glucose uptake, is suppressed, this occurs. The goal of this study is to review past research on the relationship between serum uric acid and diabetes type II in various parts of the world, as well as the prevalence of such a link. Articles were chosen using the PubMed database and EBSCO Information Services. We used all relevant publications to our review that dealt with the connection among both serum uric acid and diabetes type II, in addition to the other articles. Other publications that were not linked to this field were excluded. In this systematic review, serum uric Acid levels were found to be correlated to type 2 diabetes mellitus, metabolic syndrome and carotid artery disease. Atherosclerosis is more common in people with type 2 diabetes. The reliability of concentrations of uric acid levels in blood in predicting type 2 diabetes and enhancing prevention should be the focus of future study.

A review on the fruit components affecting uric acid level and their underlying mechanisms.

Uric acid (UA) is produced in the liver and excreted through the kidneys and intestines. If UA is overproduced or its excretion reduces, the concentration of UA increases, leading to hyperuricemia and gout. The high concentration of UA is also related to cardiovascular disease, hypertension, obesity, and other diseases. Fruits are healthy foods. However, fruits contain fructose and small amounts of purine, and the product of their metabolism is UA. Therefore, theoretically, eating fruits will increase the concentration of serum UA. Fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In addition to the UA synthesized by fructose and purine metabolism, the mechanisms by which other components affect the concentration of serum UA can be summarized as follows: (a) inhibiting xanthine oxidase; (b) reducing reabsorption of UA; and (c) improving the excretion of UA. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations, and explained their mechanisms for the first time, which references for patients with hyperuricemia to take fruits. PRACTICAL APPLICATIONS: With the rising prevalence, hyperuricemia and gout have become public health problems that endanger our daily life. The key to the treatment of hyperuricemia is to control the level of serum UA within the normal range. Fruits are healthy foods. However, fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations. We also explained their mechanisms, which references for patients with hyperuricemia to take fruits.

CRISPR-Cas9-mediated reactivation of the uricase pseudogene in human cells prevents acute hyperuricemia

The utility of CRISPR-Cas9 to repair or reverse diseased states that arise from recent genetic mutations in the human genome is now widely appreciated. The use of CRISPR to “design” the outcomes of biology is challenged by both specialized ethicists and the general public. Less of a focus, however, is the ability of CRISPR to provide metabolic supplements or prophylactic molecules that improve long-term human health by overwriting ancient evolutionary events. Here, we use CRISPR to genomically integrate a functional uricase gene that encodes an enzymatically active protein into the human genome. These uricase-producing cells are able to reduce or even eliminate high concentrations of exogenous uric acid despite the enzyme being localized to peroxisomes. Our evolutionary engineered cells represent the first instance of the primate ape lineage expressing a functional uricase encoded in the genome within the last 20 million years. We anticipate that human cells expressing uricase will help prevent hyperuricemia (including gout) as well as hypertension and will help protect against fatty liver disease in the future.