Acid Levels In Individuals Research Articles

Comprehensive Assessment of Albumin and Uric Acid Levels in Oral Submucous Fibrosis: A Comparative Case-Control Study Involving Different Risk Groups.

Background Oral submucous fibrosis (OSMF) is a premalignant disorder that impacts the oral cavity and pharynx. Major risk factors for OSMF are attributed to the consumption of betel nuts or tobacco. These substances harbor various carcinogens that trigger the production of free radicals and reactive oxygen species. Antioxidants are pivotal in preserving cellular integrity and impeding the oncogenic transformation of body cells. In this context, albumin and uric acid, being primary antioxidants present in body fluids, bestow a defensive effect against this condition. Thus, the present study is designed to elucidate the differential concentration of albumin and uric acid between patient cases and healthy cohorts. Methodology This case-control study was conducted to evaluate the albumin and uric acid levels in individuals diagnosed with OSMF (cases) and compare them with healthy controls for a period of six months. A cohort of 100 individuals was partitioned into four groups, with each group comprising 25 individuals: Group I was made up of healthy individuals; Group II consisted of individuals who chew tobacco and areca nuts but are not affected by OSMF; Group III included individuals who only use tobacco without areca nuts and are afflicted with OSMF; and Group IV comprised individuals who consume a combination of areca nuts and tobacco and are diagnosed with OSMF. Biochemical evaluation was carried out using the BS-380 chemistry autoanalyzer (Mindray, Shenzhen, China), and the quantification of serum albumin and uric acid was performed by the uricase-peroxidase (POD) method with dihydroxybenzene sulfonic acid (DHBS). Results The study cohort of 100 individuals was made up of 70 males and 30 females, with an average age of 42.51 (11.62) years. The comparison of the mean concentration of serum albumin across all groups revealed that healthy controls exhibited the highest serum albumin concentration of 4.284 (0.618), with a statistically significant p-value (0.001) across all groups. A comparison of the mean value of serum uric acid among all groups showed that healthy controls had the highest value of serum uric acid (5.26±1.161), with a considerable p-value (0.001) between all groups. Conclusion The present study concluded that serum biomarkers assessed were high in healthy individuals and consumption of areca nuts, tobacco, and their products was significantly associated with low levels of albumin and uric acid. Therefore, both albumin and uric acid can be used as important biomarkers for uncovering oral premalignant lesions and conditions ahead of time and can also be used in mass screening.

Investigation of Serum Uric Acid Levels in Individuals Eating Different Diets

Investigation of Serum Uric Acid Levels in Individuals Eating Different Diets

Association of obesity with serum free fatty acid levels in individuals at different stages of prediabetes

We investigated the associations of prediabetes categories and obesity with serum free fatty acid (FFA) levels and adipose tissue insulin resistance. This study included 5006 male participants (1779, 1025, 629, 874, and 699 with normal fasting glucose/normal glucose tolerance, isolated impaired fasting glucose [IFG], isolated impaired glucose tolerance [IGT], IFG plus IGT, and diabetes, respectively). Serum FFA levels were assessed before and 30, 60, and 120 min after glucose ingestion, and the total area under the FFA curve (AUCFFA ) was calculated. Adipose insulin resistance index (adipo-IR) was assessed based on fasting FFA and insulin concentrations. Isolated IFG was associated with high fasting FFA levels (OR, 1.35; p < 0.001) and high adipo-IR (OR, 1.82; p < 0.001) only in the nonobesity group. Isolated IGT, IFG plus IGT, and diabetes were associated with high fasting FFA levels, regardless of obesity. Obesity was significantly associated with AUCFFA , and the duration of obesity-related impairment in lipolysis inhibition after glucose ingestion was prolonged in IFG plus IGT and diabetes. These results suggest that IFG and obesity may overlap in their effects on FFA metabolism whereas IGT has significant effects on FFA independent of obesity. Obesity impact on lipolysis may be involved in worsening glucose metabolism.

Plasma amino acid levels in individuals with bacterial pneumonia and healthy controls.

Amino acids play an important role in immune responses and as neurotransmitters. During the course of a bacterial pneumonia episode, from the onset to the recovery phase, immune responses dramatically change, as does the metabolism of amino acids, a concept referred to as immuno-nutrition. We investigated the differences in plasma amino acid levels (PAA) between the acute and recovery phases in individuals with community-acquired pneumonia (CAP) and healthy controls. Two groups of participants were recruited: Healthy adults aged over 60 years and patients hospitalized with CAP. Samples were collected on Day 0 (the day of admission) and Day 7 (after 6-8 days treatment). A total of 93 healthy adults and 60 patients with CAP participated in the study. Of those with CAP, 43 had their amino acids measured on Day 7. Patients with CAP had markedly decreased PAA of 12 amino acids on Day 0. Citrulline, histidine, and tryptophan remained low in male, while aspartic acid, asparagine, ornithine, proline, and threonine were higher on Day 7 in both males and females. Phenylalanine increased at Day 0 and Day7. The findings suggest that the host response against bacterial infection changed the plasma amino acid levels. PAA on Day 7 (representing convalescence) continued to display an amino acid profile distinct from that observed in healthy individuals. Based on these findings, reconsideration for providing amino acids to patients with bacterial pneumonia should be needed depending on stage of the pneumonia from the perspective of immuno-nutrition.

Neurotransmitter Precursor Amino Acid Ratios Show Differential, Inverse Correlations with Depression Severity in the Low and High Depression Score Range.

The immunomodulatory capacity of mental stress is one of the basic concepts of psychoneuroimmunology. The current prospective longitudinal study was designed to evaluate the effect of acute mental stress on neurotransmitter precursor amino acid levels in individuals with depression at 2 time points. Ten physically healthy patients with a diagnosis of major depressive episode and Montgomery–Åsberg Depression Rating Scale scores (MADRAS) ⩾20 points at inclusion were assessed on 2 study days (once with higher MADRAS scores, once with lower MADRAS scores; median 34.5 days apart) and subjected to a standardized acute mental stress test on each study day. Blood was collected at 4 time points: once prior to and at 3 time points (0, 30 minutes, 60 minutes) following mental stress. Neurotransmitter precursor amino acid levels, that is kynurenine/tryptophan (KYN/TRP) and phenylalanine/tyrosine (PHE/TYR), as well as neopterin and nitrite were analyzed in a total of 80 individual blood samples. Regression and correlation analyses were performed. Regression analyses of PHE/TYR (R2 = .547) and KYN/TRP (R2 = .440) in relation to MADRAS depression severity showed a quadratic curve fit. This was reflected by a negative linear correlation between MADRAS scores and PHE/TYR as well as KYN/TRP in the lower score range (r = −.805, P < .001 and r = −.586, P < .001 respectively) and a positive correlation in the higher MADRAS score range (r = .713, P < .001 and r = .379, P = .016 respectively). No effect of acute mental stress was found. This analysis exemplifies the implications of sampling as well as data distributions on results. The crosstalk of biological mechanisms that orchestrate metabolic and immunological signaling may vary depending on depression severity resulting in non-linear associations that may explain the heterogeneity of results found in the literature.

Elevated plasma free sialic acid levels in individuals with reduced glomerular filtration rates.

N-acetylneuraminic acid (Neu5Ac, sialic acid) is a negatively charged monosaccharide, and the predominant form of sialic acid in human cells (1). Sialic acid is typically found as the terminal monosaccharide on glycoconjugates, where it plays a role in various physiologic and pathologic interactions (1). Sialylated glycoconjugates are critical contributors to the polyanionic component of the glomerular glycocalyx, contributing to size and charge selectivity for plasma macromolecules (1,2). Podocyte foot process morphology is maintained by the anionic charged sialic acid residues on glycoconjugates in podocyte membranes (2). Free sialic acid is filtered but not reabsorbed by the human kidney, in a fashion similar to that for creatinine (3), but in contrast to the handling of other monosaccharides such as glucose, mannose, galactose, and fructose that are reabsorbed by tubular cells (4). Circulating sialic acid levels, both unbound and bound to glycoconjugates, have only been sporadically studied in different conditions, including some renal disorders (3,5−9); a possible causative link to reduced eGFRs has been seldom discussed or investigated. We designed this study to establish a correlation between eGFR and plasma free sialic acid across a range of subjects with glomerular disorders. This would not only emphasize this often-overlooked aspect of renal filtering of free sialic acid, but also inform our developmental program for glomerular diseases using the sialic acid precursor, N-acetylmannosamine (ManNAc) (10), which was expected to significantly increase plasma free sialic acid levels in subjects with reduced eGFR. Peripheral blood was obtained from eight subjects enrolled in National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) natural history study 94-DK-0127 (ClinicalTrials.gov identifier, NT1392), “Pathogenesis of FSGS,” and from eight subjects enrolled in NIDDK study 16-DK-0036 (ClinicalTrials.gov identifier, NCT02639260), “A Phase 1 Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of …

Cerebral Glutamate and Gamma-Aminobutyric Acid Levels in Individuals at Ultra-high Risk for Psychosis and the Association With Clinical Symptoms and Cognition

BackgroundStudies examining glutamate or gamma-aminobutyric acid (GABA) in ultra-high risk for psychosis (UHR) and the association with pathophysiology and cognition have shown conflicting results. We aimed to determine whether perturbed glutamate and GABA levels in the anterior cingulate cortex and glutamate levels in the left thalamus were present in UHR individuals and to investigate associations between metabolite levels and clinical symptoms and cognition. MethodsWe included 122 UHR individuals and 60 healthy control subjects. Participants underwent proton magnetic resonance spectroscopy to estimate glutamate and GABA levels and undertook clinical and cognitive assessments. ResultsWe found no differences in metabolite levels between UHR individuals and healthy control subjects. In UHR individuals, we found negative correlations in the anterior cingulate cortex between the composite of glutamate and glutamine (Glx) and the Comprehensive Assessment of At-Risk Mental States composite score (p = .04) and between GABA and alogia (p = .01); positive associations in the anterior cingulate cortex between glutamate (p = .01) and Glx (p = .01) and spatial working memory and between glutamate (p = .04), Glx (p = .04), and GABA (p = .02) and set-shifting; and a positive association in the thalamus between glutamate and attention (p = .04). No associations between metabolites and clinical or cognitive scores were found in the healthy control subjects. ConclusionsAn association between glutamate and GABA levels and clinical symptoms and cognition found only in UHR individuals suggests a loss of the normal relationship between metabolite levels and cognitive function. Longitudinal studies with investigation of clinical and cognitive outcome and the association with baseline levels of glutamate and GABA could illuminate whether glutamatergic and GABAergic dysfunction predicts clinical outcome.

The Dietary Approaches to Stop Hypertension (DASH) diet, Western diet, and risk of gout in men: prospective cohort study

Objective To prospectively examine the relation between the Dietary Approaches to Stop Hypertension (DASH) and Western diets and risk of gout (ie, the clinical endpoint of hyperuricemia) in men.Design Prospective...

Serum Sialic Acid Levels in Individuals with or without Iron Deficiency Anemia

Amac : Bu calismanin amaci demir eksikligi anemisi (DEA) parametreleri ile serum total sialik asit (SA) degerleri arasindaki iliskinin incelenmesidir. Yontemler : Calismada DEA olan 30 hasta ve 30 saglikli kiside serum total SA, hemogram, demir, demir baglama, ferritin, C-reaktif protein (CRP) duzeylerine bakildi ve periferik yayma yapildi. Istatistiksel analizler windows programinda SPSS 20.0 (Statistical Package for Social Sciences Inc, IL, USA) ile gerceklestirildi. Normal dagilima uygun degiskenler icin bagimsiz orneklem t testi ve Pearson korelasyon analizi, uygun olmayanlar icin ise Mann-Whitney U testi ve Spearman sira korelasyon analizi uygulandi. Bulgular : Gruplar arasinda istatistiksel olarak yas farki gorulmedi (p>0,05). Hasta grubu, kontrol grubu ile kiyaslandiginda istatistiksel olarak; hemoglobin, hematokrit, eritrositlerin ortalama buyuklugu (MCV), ortalama eritrosit hemoglobin miktari (MCH), ve ferritin degerleri anlamli olarak (p 0,05). CRP ve SA degerleri arasinda korelasyon saptanmamistir (r=0,110, p=0,561). Sonuc : DEA’de serum total SA degerleri, DEA olmayan kontrol grubuna gore yuksek bulunmustur. Daha onceki calismalarda farkli hastalik gruplarinda SA yuksekligi inflamasyon varligina baglanmistir. Calismamizda, hasta ve kontrol grubu arasinda CRP degerlerinde bir fark olmadigi goz onune alindiginda, bu artmanin nedeninin akut faz proteini olarak degerlendirilen ve SA iceren proteinlerden kaynaklanmadigini dusunmekteyiz.

Down-regulation of a signaling mediator in association with lowered plasma arachidonic acid levels in individuals with autism spectrum disorders

Previous studies have indicated that the altered composition of polyunsaturated fatty acids (PUFAs) might contribute to the pathophysiology of autism spectrum disorder (ASD). We examined the relationship between the plasma fatty acid levels, expressed as μg/ml, and the plasma levels of biomarkers of AA-related signaling mediators, such as ceruloplasmin, transferrin and superoxide dismutase, and assessed the behavioral symptoms of 30 individuals with ASD (mean age, 13.6 ± 4.3 years old) compared with 20 age- and gender-matched normal controls (mean age, 13.2 ± 5.4 years old) using Aberrant Behavior Checklists (ABC). The plasma levels of EPA and the plasma ratios of EPA/AA were significantly higher, while the plasma levels of AA and metabolites, such as 5,8,11,14-eicosatetraenoic acid, adrenic acid, and ceruloplasmin (Cp), were significantly lower in the 30 individuals with ASD compared with the 20 normal controls. The ABC scores were significantly increased in the ASD group compared with those of the control group. Thus, the results of the present study revealed that reduced plasma levels of AA and metabolites in association with high plasma EPA/AA ratios might down-regulate AA-related signaling mediators, such as Cp. Subsequently, reduced plasma Cp levels might reduce the protective capacity for brain damage, resulting in the pathophysiology underlying the behavioral symptoms in individuals with ASD. These findings suggest that reduced plasma AA levels may downregulate Cp.

Common Variants in LRP2 and COMT Genes Affect the Susceptibility of Gout in a Chinese Population.

Gout is a common inflammation disease resulting from an increase in serum uric acid. Nearly 70% of uric acid is excreted via the kidneys. To date, evidence for an association between genetic loci and gout is absent, equivocal or not replicated. Our study aims to test variants in two genes abundantly expressed in the kidney, LRP2 and COMT, for their association with uric acid and gout. In total, 1318 Chinese individuals were genotyped for rs2544390 in LRP2 and rs4680 in COMT. These LRP2 and COMT gene polymorphisms showed no significant effect on uric acid (P = 0.204 and 0.188, separately); however, rs2544390 in LRP2 did influence uric acid levels in individuals with BMI ≥ 25 (P = 0.009). In addition, the allele frequency distributions of the two loci showed a significant difference between gout patients and healthy controls. A missense variation in rs4680 (G > A) decreased the risk of gout (OR = 0.77, P = 0.015), whereas the T allele of rs2544390 was associated with gout pathogenesis risk (OR = 1.26, P = 0.020). The present study provides the first evidence for an association between COMT and gout. Rs2544390 in LRP2 only influenced uric acid levels in individuals with BMI ≥ 25, which might explain the discrepant results among previous studies. In addition, we are the first to identify the association between LRP2 and gout in a Chinese population and to confirm this association in Asians.

Correlates of electroencephalographic resting states and erythrocyte membrane docosahexaenoic and eicosapentaenoic acid levels in individuals at ultra-high risk of psychosis.

Abnormal levels of polyunsaturated fatty acids (PUFAs) have been reported in individuals suffering from schizophrenia. The main aim of the present study was to investigate the relationship between erythrocyte membrane fatty acid levels and resting-state brain activity occurring in individuals at ultra-high risk (UHR) of psychosis. The association between erythrocyte membrane fatty acids levels and resting-state brain activity and its value in predicting psychosis was examined in 72 UHR individuals. In the frontal area, the activity in the fast frequency band Beta2 was positively associated with docosahexaenoic acid (DHA) levels (R = 0.321, P = 0.017), and in the fronto-central area, Beta2 activity showed a positive correlation with eicosapentaenoic acid (EPA) levels (R = 0.305, P = 0.009), regardless of psychosis transition status. Conversely, the slow frequency band Theta was significantly negatively associated with EPA levels in the parieto-occipital region (R = -0.251, P = 0.033. Results also showed that Alpha power was negatively correlated with DHA levels in UHR individuals who did not transition to psychosis, while this correlation was not present in individuals who later transitioned. Our results suggest that individuals at UHR for psychosis who have higher basal omega-3 fatty acids levels present with resting EEG features associated with better states of alertness and vigilance. Furthermore, the improvement in the Alpha synchrony observed along with increased DHA levels in participants who did not transition to psychosis is disturbed in those who did transition. However, these interesting results are limited by the small sample size and low statistical power of the study.

Markers of and Risk Factors for the Development and Progression of Diabetic Kidney Disease

Diabetic kidney disease (DKD) occurs in 25%-40% of patients with diabetes. Given the dual problems of a significant risk of progression from DKD to end-stage renal disease (ESRD) and increased cardiovascular morbidity and mortality, it is important to identify patients at risk of DKD and ESRD and initiate protective renal and cardiovascular therapies. The importance of preventive therapy is emphasized further by worldwide increases in the incidence of diabetes. This review summarizes the evidence regarding the prognostic value and benefits of targeting established and novel risk markers for DKD development and progression. Family history of DKD, smoking history, and glycemic, blood pressure, and plasma lipid level control are established factors for identifying people at greatest risk of DKD development and progression. Absolute albumin excretion rate (AER) and glomerular filtration rate (GFR) measurements also are important, although AER categorization generally lacks the necessary specificity and sensitivity, and estimates of declining GFR are compromised by methodological limitations for GFRs in the normal-to-high range. Emerging risk markers for progressive loss of kidney function include markers of oxidation and inflammation, profibrotic cytokines, uric acid, advanced glycation end products, functional and structural markers of vascular dysfunction, kidney structural changes, and tubular biomarkers. Among these, the most promising are serum uric acid and soluble tumor necrosis factor receptor (type 1 and type 2) levels, especially in relation to GFR changes. At present, these can only be considered as risk markers because they only identify an individual at increased risk of progressive DKD and not necessarily related to the causal pathway promoting kidney damage. Further work is needed to establish whether modulating these factors improves the prognosis in DKD. Although change in urinary peptidome levels also is a promising marker, there currently is neither a clinical assay nor adequate studies defining its prognostic value. Until these or other novel markers become available for clinical use, predictive accuracy often may be increased with greater attention to established markers.

Effect of baseline plasma fatty acids on eicosapentaenoic acid levels in individuals supplemented with α-linolenic acid

We previously reported a >50% increase in mean plasma eicosapentaenoic acid levels in a general medicine clinic population after supplementation with α-linolenic acid. In the current analysis, we evaluate the variability of changes in eicosapentaenoic acid levels among individuals supplemented with α-linolenic acid and evaluated the impact of baseline plasma fatty acids levels on changes in eicosapentaenoic acid levels in these individuals. Changes in eicosapentaenoic acid levels among individuals supplemented with α-linolenic acid ranged from a 55% decrease to a 967% increase. Baseline plasma fatty acids had no statistically significant effect on changes in eicosapentaenoic levels acid after α-linolenic acid supplementation. Changes in eicosapentaenoic acid levels varied considerably in a general internal medicine clinic population supplemented with α-linolenic acid. Factors that may impact changes in plasma eicosapentaenoic acid levels after α-linolenic acid supplementation warrant further study.

Decreased Urinary Uronic Acid Levels in Individuals with Interstitial Cystitis

The pathogenesis of interstitial cystitis currently is unknown. A possible etiology is that the transitional epithelium is defective, leading to molecular leaks that initiate the disease complex. An important surface defense mechanism is the glycosaminoglycans or polysaccharides that line the bladder epithelium and act as a nonspecific antiadherence factor blocking access of bacteria, microcrystals, proteins and ions to the underlying transitional cells. We examined the excretion of urinary macromolecular uronic acid and glycosaminoglycans in normal individuals and those with interstitial cystitis. A total of 37 controls had a mean macromolecular uronic acid level of 56nmol, per mg. creatinine, compared to 40.2nmol, per mg. creatinine in 43 patients with active disease (differences were significant, p equals 0.03). The median excretions of glycosaminoglycan uronate for controls and patients were 15.1 and 11.1nmol, per mg. creatinine, respectively. (There was an over-all tendency to decrease excretion in patients with a p value of 0.06.) Specimens obtained at cystoscopy from patients with active interstitial cystitis had ureteral macromolecular uronic acid levels of 40.5nmol, uronate per mg. creatinine compared to 43.6nmol, uronate per mg. creatinine from the bladder. Interstitial cystitis patients had 16.0nmol, glycosaminoglycan uronate per mg. creatinine compared to 14.6nmol, per mg. creatinine in normal controls. Neither of these differences was statistically significant. It would appear that there is a tendency to lower macromolecular uronic acid and polysaccharide excretion in individuals afflicted with this syndrome.

Familial hyper- and hypouricemias in random and hyperlipidemic recall cohorts: The Princeton School District Family Study

Using the Princeton School Family Study, our specific aim was to estimate the prevalence of familial hyper- and hypouricemia, to estimate the proportion of probands' first-degree relatives who were similarly affected, and to evaluate the contribution of diseases, drugs, and alcohol intake (if any) to uric acid levels. We studied 379 probands and a total of 1928 subjects, 125 and 52 black probands from a randomly recalled group, 147 white and 55 black probands from a hyperlipidemic recall (top decile cholesterol and/or triglyceride) group. Familial hyper- and hypouricemias were arbitrarily identified in those kindreds having at least two first-degree relatives in the same decile as the proband, top or bottom respectively, for serum uric acid. No probands had symptomatic gout. Diseases, drugs, and alcohol intake were not consistently associated with aggregations of high and/or low uric acid levels in families, and had little relationship to uric acid levels in individuals. Of the 177 randomly recalled probands, and of the 55 black probands in hyperlipidemic recall group, none had familial hyperuricemia. Of the 147 white hyperlipidemic recall group probands and their kindreds, 2 had familial hyperuricemia, with concurrent primary hyperlipoproteinemia and hypertension. Familial hypouricemia was present in 1 of 125 white and in 1 of 52 randomly recalled black kindreds, and in 3 of 147 white and 3 of 55 hyperlipidemic recall black kindreds. While familial clustering of hyperuricemia was limited, clustering of hypouricemia was much more marked. Seventy-four and 84% respectively of first-degree relatives of hypouricemic white and black probands had uric acid < the 50th percentile. In randomly recalled probands and their first-degree relatives there were significant inverse partial correlations between uric acid and high density lipoprotein cholesterol. Inverse associations of uric acid with high density lipoprotein cholesterol and the concurrence of hyperlipoproteinemia and hypertension in hyperuricemic families points to the importance of lipoprotein and blood pressure screening in families with asymptomatic hyperuricemia. The potential ramifications of within-family clustering of hypouricemia need to be further assessed in populations, particularly in regards to uric acid nephrolithiasis.