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Academic literature on the topic 'Uric acid increases'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Uric acid increases"

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Menon, R. K., D. P. Mikhailidis, J. L. Bell, P. B. Kernoff, and P. Dandona. "Warfarin administration increases uric acid concentrations in plasma." Clinical Chemistry 32, no. 8 (August 1, 1986): 1557–59. http://dx.doi.org/10.1093/clinchem/32.8.1557.

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Abstract The effect of warfarin administration on plasma uric acid was investigated. A representative sample of patients on long-term warfarin treatment had a significantly higher concentration of uric acid in plasma than did age-matched patients with comparable plasma urea concentrations who were not taking warfarin. In women, this association was observed only in patients with normal values for plasma urea, not in those with high values. In contrast, in men this association was present in both groups (normal and high plasma urea). In a longitudinal study involving patients, their plasma uric acid significantly increased after warfarin administration. There was no significant change in the renal clearance of uric acid after a single dose of warfarin in normal, healthy volunteers; this contrasts with the increase observed with other coumarin anticoagulants. Our findings suggest that the increase in plasma uric acid noted with warfarin administration is probably due to an increase in uric acid production and may predispose to gout those patients who are on long-term therapy with warfarin.
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Kakutani-Hatayama, Miki, Manabu Kadoya, Hirokazu Okazaki, Masafumi Kurajoh, Takuhito Shoji, Hidenori Koyama, Zenta Tsutsumi, Yuji Moriwaki, Mitsuyoshi Namba, and Tetsuya Yamamoto. "Nonpharmacological Management of Gout and Hyperuricemia: Hints for Better Lifestyle." American Journal of Lifestyle Medicine 11, no. 4 (September 2, 2015): 321–29. http://dx.doi.org/10.1177/1559827615601973.

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We reviewed lifestyle factors that influence serum uric acid levels and risk of gout flare, and how to improve their deleterious effects. Since obesity increases uric acid and weight gain increases gout risk, weight reduction by daily exercise and limiting intake of excess calories is recommended. However, strenuous exercise, which causes adenine nucleotide degradation; starvation, which decreases uric acid excretion; and dehydration may raise the level of uric acid in serum and trigger gout. Increased intake of purine-rich foods, such as meat and seafood, raise the level of uric acid in serum and is associated with increased risk of gout, whereas dairy products, especially low-fat types, are associated with a lower risk of gout. Also, heavy alcohol drinking raises the uric acid level and increases the risk of gout through adenine nucleotide degradation and lactate production. Sweet fruits and soft drinks containing fructose should be moderated, since fructose may raise uric acid and increase gout risk through uric acid production and/or decreased excretion. On the other hand, the Mediterranean diet is recommended for gout patients, since it may also help prevent hyperuricemia. Furthermore, coffee and vitamin C supplementation could be considered as preventive measures, as those can lower serum uric acid levels as well as the risk of gout.
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Masuda, Akira, Takehisa Asahi, Midori Sakamaki, Katsuhito Nakamaru, Koki Hirota, and Yusuke Ito. "Uric Acid Excretion Increases During Propofol Anesthesia." Anesthesia & Analgesia 85, no. 1 (July 1997): 144–48. http://dx.doi.org/10.1097/00000539-199707000-00026.

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Masuda, Akira, Takehisa Asahi, Midori Sakamaki, Katsuhito Nakamaru, Koki Hirota, and Yusuke Ito. "Uric Acid Excretion Increases During Propofol Anesthesia." Anesthesia & Analgesia 85, no. 1 (July 1997): 144–48. http://dx.doi.org/10.1213/00000539-199707000-00026.

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Balasubramanian, T. "Uric Acid or 1-Methyl Uric Acid in the Urinary Bladder Increases Serum Glucose, Insulin, True Triglyceride, and Total Cholesterol Levels in Wistar Rats." Scientific World JOURNAL 3 (2003): 930–36. http://dx.doi.org/10.1100/tsw.2003.90.

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In animals deprived of food for a long period, a drop in the fat mass below 5% of the total body mass results in an increase in blood glucocorticoids and uric acid levels, followed by foraging activity. Since the glucocorticoids increase the uric acid excretion, an increase in the level of uric acid in the bladder urine could be the signal for this feeding behaviour and subsequent fat storage. Accumulation of fat is associated with hyperglycaemia, hyperinsulinaemia, hyperlipidaemia, and hypercholesterolaemia as seen in the metabolic syndrome or hibernation. It is hypothesized that uric acid or its structurally related compound, 1-methyl uric acid (one of the metabolites of the methyl xanthines namely caffeine, theophylline, and theobromine present in coffee, tea, cocoa, and some drugs), can act on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels. In rats, perfusion of the urinary bladder with saturated aqueous solution of uric acid or 1-methyl uric acid results in a significant increase in the serum levels of glucose, insulin, true triglyceride, and total cholesterol in comparison with perfusion of the bladder with distilled water at 20, 40, and 80 min. The uric acid or the 1-methyl uric acid acts on the urinary bladder mucosa and increases the serum glucose, insulin, true triglyceride, and total cholesterol levels.
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Sayfutdinova, L. N., and M. A. Derkho. "BLOOD PROTEINS AND THEIR INFORMATIVENESS IN ASSESSING THE ADAPTIVE RESOURCES OF CHICKENS UNDER TECHNOLOGICAL STRESS." Scientific Notes Kazan Bauman State Academy of Veterinary Medicine 245, no. 1 (March 1, 2021): 169–76. http://dx.doi.org/10.31588/2413-4201-1883-245-1-169-176.

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In the body of chickens, when exposed to the technological factor (the density of birds in the cage), a stress reaction developed as a result of activation of the hypathalamic-pituitary-adrenal system. The response and state of the neuroendocrine pathway is associated with the magnitude of the technological stress factor. When it is increased by 1.50 times, the maximum changes in the body of chickens are detected 4 hours after the start of the experiment. At the same time, the level of corticosterone and cortisol in the blood of birds increases by 3.42 and 2.99 times, increasing the rate of catabolic reactions in protein metabolism. Therefore, the amount of total protein in the blood-stream of chickens increases by 34.32 %, albumins by 26.74 %, urea and uric acid by 2.07 and 2.29 times, and the activity of AsAT and AlAT increases by 2.15 and 4.53 times (p<0.05). The catabolic processes involve mainly blood albumins, whose nitrogen is used for the synthesis of uric acid. This is evidenced by a decrease in the value of Alb/uric acid by 42.74 % (p<0.05). With an increase in the density of birds in the cage by 2 times, the reaction of the GGNS more pronounced and long-lasting. Although the maximum changes are registered 2 hours after the initiation of stress, they per-sist throughout the study period. At the same time, the level of corticosterone and cortisol in the blood of chickens increases by 4.17 and 3.67 times, the concentration of total protein by 39.44 %, both due to albumins (by 41.78 %) and globulins (by 37.82 %); the increase in the amount of urea and uric acid is 2.18 and 2.45 times. Both albumins and blood globulins are subjected to oxidative decomposition, which determines the decrease in the ratio TP/Urea, Alb/urea at, TP/uric acid and Alb/uric acid at 35.72-43.18 %. At the same time, the activity of AlAT increases by 7.56 times and AsAT by 2.21 times, determining the predominant use of carbon residues of free amino acids in the processes of gluconeogenesis (AlAT/AsAT increased by 3.75 times).
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Mass, Baba, Brea Nance, and Saroja Voruganti. "Fructose Increases the Expression of Uric Acid-Induced Oxidative Stress Genes, NOX4 and FOXO3, in Cultured HepG2 Cells." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1266. http://dx.doi.org/10.1093/cdn/nzaa058_024.

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Abstract Objectives Uric acid is the final product of purine metabolism. The role of uric acid in oxidative stress is not clear. Studies have shown uric acid as antioxidant as well as pro-oxidant. High fructose sugar consumption increases uric acid levels by ATP depletion and the subsequent formation AMP which is a uric acid precursor. In our study, we investigated the effect of dose dependent treatments of fructose, uric acid, or a combination of both uric acid and fructose on expression of oxidative stress-related genes, mainly NADPH oxidase 4 (NOX4), superoxide dismutase 3 (SOD3), Forkhead Box O3 (FOXO3) and xanthine dehydrogenase (XDH) in cultured Hep G2 cells. Methods Human hepatocellular carcinoma [HEPG2] (ATCC HB8065) cells were treated with serum-free medium containing either 10 mM fructose, soluble uric acid (0.25 mM, 0.5 mM, or 0.75 mM), or a combination of fructose and uric acid. The cells were collected at the end of each incubation period (30 min, 2 and 24 hours) to extract total RNA. cDNA was synthesized from the extracted RNA. TaqMan assays were designed for use on real-rime PCR platform (QuantStudio 12 K Flex). TaqMan open array primers were custom-made by Thermo Fisher Scientific. Target quantification values were normalized against GAPDH levels and a combination of students’ t-test and ANOVA were applied. Results Soluble uric acid, either by itself or in conjunction with fructose, did not change the expression of the tested genes at 30 minutes or 2 hours. However, after 24 hours of incubation, uric acid increased the expression of NOX4 by 2 and FOXO3 by 1.5-fold (p &lt; 0.05) whereas uric acid plus fructose-containing media increased the expression of NOX4 by 3.5 and FOXO3 by 2-fold (p &lt; 0.05) after 24 hours of incubation as compared to control. No treatment differences were observed in the expression of SOD3. Conclusions These findings demonstrate that fructose increases the expression of uric acid-induced oxidative stress related genes. Funding Sources None.
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Karwur, Ferry Fredy, and Dwi Rahayu Pujiastuti. "Review Article: URIC ACID HOMEOSTASIS AND DISTURBANCES." Folia Medica Indonesiana 53, no. 4 (December 28, 2017): 292. http://dx.doi.org/10.20473/fmi.v53i4.7164.

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This review examined the homeostasis of uric acid in human body and analyzed recent studies of the affecting major variables. Normal uric acid concentration in male is 3.5-7.2 mg/dL and in female is 2.6-6 mg/dL. Daily turnover of normal uric acid ranges from 498-1392 mg/day, miscible pool is 767-1650 mg, reabsorption is 8064 mg/day, renal excretion is 262-620 mg/day and intestine 186-313 mg/day. The dynamics of uric acid is influenced by factors of food, drink, age, history of disease, and genetic. High purine dietary consumption increases blood uric acid by 1-2 mg/dL, 213-290 g/day fructose drinks increases 0.52-1.7 mg/dL, 1.5 g/kgBW sucrose increases 0.61 mg/dL, and 10-20 ml/kgBW beer increases 0.50-0.92 mg/dL. The ABCG2 gene plays a role in bringing uric acid out of the body by 114.31-162.73 mg/dL, SLC2A9 of 5.43-20.17 mg/dL, and SLC22A12 of 5.77-6.71 mg/dL. The data described the homeostasis of uric acid and the magnitude of the impact of environmental (consumption of food, beverages, and lifestyle) and genetic factors. Understanding uric acid homeostasis and its disturbances is important in managing diseases as a consequence of hyperuricemia and hypouryscemia
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Pandey, Rachana, Sanjaya Humagain, Prabodh Risal, Rahul Kumar Yadav, and Buddhi Raj Pokhrel. "Association between Serum Uric Acid and Blood Glucose Level in Diabetic and Non-diabetic Patients." Nepal Medical College Journal 24, no. 4 (December 23, 2022): 271–75. http://dx.doi.org/10.3126/nmcj.v24i4.50576.

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Uric acid increases insulin resistance; likewise, hyperinsulinemia increases uric acid concentration, and both are global health problems. This study is conducted to find the association between serum uric acid and blood glucose level. This was a cross-sectional study conducted in the Department of Biochemistry and Internal Medicine at Dhulikhel Hospital, Nepal, for a duration of six months (September 2021 - February 2022). A total of 130 diabetic patients who consented were compared with 130 non-diabetics by using non-probability convenient sampling technique. Ethical clearance was taken from the Institutional Review Committee-Kathmandu University School of Medical Sciences. Venous blood was collected and fasting blood glucose, post-prandial blood glucose, and serum uric acid were measured. Data were analyzed in the Statistical Package for Social version 16.0. Analytical data were compared using Mann Whitney U test, and Spearman correlation was performed to correlate numerical parameters. Statistical significance was defined as a two-sided p-value of less than 0.05. The median of serum uric acid level was significantly higher in diabetics than non-diabetics; the level of fasting and post-prandial blood glucose positively correlated with serum uric acid (p<0.05). Hyperuricemia was more in diabetics than non-diabetics (p<0.05). Serum uric acid level increased with the increase in age and duration of diabetes.
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Liu, S., and J. N. Miner. "THU0534 Skipping Breakfast Increases Serum Uric Acid Levels." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 385.1–385. http://dx.doi.org/10.1136/annrheumdis-2016-eular.1792.

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Books on the topic "Uric acid increases"

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Daudon, Michel, and Paul Jungers. Uric acid stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0202_update_001.

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Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°C, UA is in non-dissociated form, whose solubility is at best 100 mg/L, whereas urinary UA excretion normally exceeds 600 mg/day and may exceed 1g/day.Because UA solubility increases up to approximately 500 mg/L at urine pH > 6, urine alkalinization, with a target pH of 6.5–7, is the cornerstone of medical treatment. This most often allows dissolution of existing stones and prevention of recurrent stone formation so that urological intervention is infrequently needed. The preferred agent for alkalinization is potassium citrate (30–60 mEq/day in divided doses), because potassium urate is twice more soluble than sodium urate. However, in patients with poor gastric tolerance to potassium citrate or contraindication to potassium supplements, sodium bicarbonate is an acceptable alternative. Limitation of animal proteins, purine-rich foods (including beer), alcoholic drinks and acidified beverages (sodas) are useful measures, together with large fluid intake (> 2–2.5 L/day). Allopurinol may be indicated in cases of symptomatic hyperuricaemia. Regular observance of alkalinisation, with periodic controls of urine pH by the patient, is needed to prevent the rapid formation of UA stones. Patients affected by UANL, especially if overweight, should be evaluated for type 2 diabetes or glucose intolerance and managed accordingly.
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Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.
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Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.
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Book chapters on the topic "Uric acid increases"

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Pelatti, A., C. P. Quaratino, C. D’ Amario, R. Tentarelli, G. Riario Sforza, and A. Giacomello. "Hypouricemia and an Increased Clearance of Uric Acid are Observed in Liver Diseases?" In Purine and Pyrimidine Metabolism in Man VIII, 57–60. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_14.

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Kogure, A., T. Harayama, Y. Takakura, T. Umekawa, K. Yoshioka, and T. Yoshida. "C677T Mutation in the Methylenetetrahydrofolate Reductase Gene Increases Serum Uric Acid in Obese Subjects." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–448—P1–448. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p9.p1-448.

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Gallo, Giuseppe. "Reducing Compounds Roles in Oxidative Stress Relieving of Human Red Blood Cells." In Reactive Oxygen Species [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99977.

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Oxidative stress is the consequence of an imbalance between pro-oxidant and antioxidant processes. Antioxidants that counteract reactive oxygen species do not all work the same way. Both resveratrol and the more powerful 4-hydroxytyrosol are excellent reducing agents. Polyphenol treatment (red wine polyphenols, resveratrol and catechin) is associated with a significant increase in anion permeability for chloride compared with control and 2.2′-azobis-2 amidinopropan dihydrochloride affected cells. Treatment with polyphenols was associated with a significant reduction in mean ± standard error of the mean membrane lipid peroxidation compared with control and 2.2′-azobis-2 amidinopropan dihydrochloride treatment. Hemolysis data are also obtained in the previously described conditions. 4-hydroxytyrosol is shown to significantly protect red blood cells from oxidative damage by 4-hydroxynonenal. But there are paradoxical effects like uric acid and creatinine. The obtained data evidence that both creatinine and uric acid levels have influence on the ratio of both malondialdehyde/protein and 4-hydroxynonenal/protein content on red blood cell ghosts, demonstrating their possible protective role against oxidative stress at low concentrations in blood and oxidizing power at higher concentrations. Finally, polyunsaturated fatty acids do not have all this reducing power.
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Conference papers on the topic "Uric acid increases"

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Petru, L., H. Hulejova, A. Mahajan, M. Herrmann, and J. Zavada. "SAT0366 Serum uric acid increases after abrogation of systemic inflammation by tnf inhibition." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6294.

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Lommatzsch, Steven E., Seong-Joo Jeong, Kenneth Davis, Rebecca Cicale, Peader G. Noone, and Isabel P. Neuringer. "Increased Uric Acid Levels Post-Lung Transplantation Are Associated With Rejection, Infection, And Renal Insufficiency." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4327.

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Caebron, J. Y., M. Joseph, H. Vorng, J. Pincemail, M. Lagaede, and A. Capron. "OXYGEN FREE RADICAL-DEPENDENT STEP IN THE CYTOTOXICITY OF DEC-TREATED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642819.

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Over the past 35 years, diethylcarbamazine (DEC) has been the most widely used agent for the treatment of filarial diseases. However, in spite of millions of individuals treated, the mode of action of this drug remained unexplained until recently when we reported that the microfilaricidal activity of DEC was mediated by blood platelets with the additional triggering of a filarial excretory antigen (FEA) (Nature, 1987).To set up the mechanism of the larvicidal action of platelets activatedby both DEC and FEA, various inhibitors of the arachidonic acid metabolism were added in the cytotoxic assay. Aspirin failed to modify the platelet activity, whilst nordihydroguaiaretic acid, esculetin, and 5,8,11,14-heneicosatetraynoic acid dose-dependently inhibited the killing of parasites. This relationship suggested the production of a putative cytotoxic lipoxygenase product. Surprisingly, no increase in oxygenated metabolites was noted both by thin layer chromatography and by high pressure liquid chromatography.Thus, we investigated the involvement of oxygen free radicals. The hydroxyl radical scavengers tested (benzoate, uric acid, mannitol, methylene blue... ) more or less inhibited the platelet killing activity. In addition, Fe2 + (down to 10-11M) enhanced the DEC-induced cytotoxicity which was abolished in the presence of the Fe2 + chelator o-phenantroline. Finally, using the electronspin resonance technique it was possible to drop OH radicals from platelets with DMPO, but only in the presence of both DEC and FEA.These results, taken with those concerning the interaction of either IgE/anti-IgE (Nature, 1983, 303, 810-812) or CRP (Science, 1986, 231, 153-156) with platelets, should be regarded as a significant insight into the involvement of platelets in various pathological processes.
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Chen, M., X. Lu, and H. Wu. "THU0048 Soluble uric acid increased the expression of ABCG2 and PDZK1 in human intestinal cell lines through the TLR4/NLRP3/CASPASE-1 and PI3K/AKT signaling pathways." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5673.

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Boelaert, J., P. Lijnen, R. Daneels, M. Schurgers, and A. Amery. "SULPHINPYRAZONE (SP) AS A CAUSE OF ACUTE RENAL FAILURE (ARF): A REVIEW." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644813.

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A total of 41 patients (all but one since 1980, 10 from our own group) have been reported with ARF due to SP. Their mean age was 58 years. 84 % of them received SP for coronary or cerebrovascular disease. Signs of pre-existing renal disease were absent in 91%of cases. Daily dosage of SP was < 400 mg in 21 %, 600 mg in 21 % and 800 mg in 58 % of the cases. ARF appeared within the first day of R/ with SP in31 % of cases(median delay of 4 days). Oliguria was present in 41 % and lumbar or abdominal pain in 26 %. Urinalysis showed uric acid crystals in 13 %. Serum creatinine peaked at a mean of 7.2 mg%. Extrarenal signs (fever, rash) were rare (10 %). 3 patients (8 %) died; renal function recovered in the others, acute dialysis being needed in 6 cases (15 %). Renal histology (11 cases) showed either no lesions (2), minimal tubulo-interstitial lesions (3), discrete interstitial infiltration (2), acute interstitial nephritis (3) or acute tubular necrosis (1).SP can cause ARF by 3 mechanisms which are not mutually exclusive : acute urate nephropathy, acute (immunological) interstitial nephritis or acute ischaemia due to inhibition of the renal synthesis of kallikrein-kinin and/or vasodilatory prostaglandins. We suggest that the latter mechanism is the most prevalent. The effect of SP on the renal prostaglandin synthesis is not settled; thurinary excretion of kallikrein is significantly depressed by SPIn conclusion : since 1980, R/ with SP is a frequent cause of ARF Practically: 1) the indications for sp should be taken with care; 2) a progressive increase in the dosage of SP may decreses the incidence of ARF.
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Triyono, Agus, Widhi Astana, Fajar Novianto, Zuraida Zulkarnain, Ulfa Fitriani, Ulfatun Nissa, and Danang Ardianto. "The Effect of Hyperuricemia Herbs Drink on the Quality of Life." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.40.

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ABSTRACT Background: The prevalence of hyperuricemia increased rapidly in recent years and has closely interdependent relationship with other metabolic disorders. Conventional medication drugs are usually associated with many side effects. About 75 to 80% of the world population use herbal medicines, mainly in developing countries, for primary health care because of their better acceptability with human body and lesser side effects. This study aimed to examine the effect of hyperuricemia herbs drink on the quality of life. Subjects and Method: A quasi experiment with no control group was carried out at Hortus Medicus clinic, Tawangmangu, Central Java. A sample of 30 hyperuricemia patients (blood uric acid 7-10 mg/dl) was selected for this study. The study subjects consume hyperuricemia herbs drink for 28 days. The dependent variable was quality of life. The independent variables were hyperuricemia herbs drink consumption. Data on quality of life were measured by Short Form-36 (SF-36). Mean difference of quality of life score before and after intervention were analyzed by independent t test. Results: Quality of life score after consuming hypercuremia herbs drink for 28 days (Mean= 80.37; SD=11.89) was higher than before (Mean= 76.20; SD= 15.08), and it was statistically significant (p= 0.001). There was no difference of quality of life score (physical function, physical role, mental health social function, and emotional role dimensions) before and after therapy. Conclusion: Hyperuricemia herbs drink for 28 days is effective to improve quality of life. Keywords: hyperurisemia herbs drink, traditional medicine, quality of life Correspondence: Agus Triyono. Research Center and Development of Traditional Medicinal and Medicinal Plants, Tawangmangu, Central Java, Indonesia. Jl. Lawu 11 Tawangmangu, Karanganyar, Central Java, Indonesia. Email: agustriyono_21@yahoo.com. Mobile: 081329038465 DOI: https://doi.org/10.26911/the7thicph.05.40
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