Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

Tissue concentrations of both homocysteine (Hcy) and cysteine (Cys) are maintained at low levels by regulated production and efficient removal of these thiols. The regulation of the metabolism of methionine and Cys is discussed from the standpoint of maintaining low levels of Hcy and Cys while, at the same time, ensuring an adequate supply of these thiols for their essential functions. S-Adenosylmethionine coordinately regulates the flux through remethylation and transsulfuration, and glycine N-methyltransferase regulates flux through transmethylation and hence the S-adenosylmethionine/S-adenosylhomocysteine ratio. Cystathionine beta-synthase activity is also regulated in response to the redox environment, and transcription of the gene is hormonally regulated in response to fuel supply (insulin, glucagon, and glucocorticoids). The H2S-producing capacity of cystathionine gamma-lyase may be regulated in response to nitric oxide. Cys is substrate for a variety of anabolic and catabolic enzymes. Its concentration is regulated primarily by hepatic Cys dioxygenase; the level of Cys dioxygenase is upregulated in a Cys-responsive manner via a decrease in the rate of polyubiquitination and, hence, degradation by the 26S proteasome.

SULFUR AMINO ACID METABOLISM: Pathways for Production and Removal of Homocysteine and Cysteine

Background Twenty-four-hour ambulatory blood pressure monitoring (ABPM) is an essential tool in the diagnosis and therapeutic monitoring of arterial hypertension in children. The statistical use of pediatric ABPM reference values has been compromised by the non-Gaussian distribution of 24-h blood pr

Distribution of 24-h ambulatory blood pressure in children: normalized reference values and role of body dimensions

Obesity, the most common nutritional disorder in industrialized countries, is associated with an increased mortality and morbidity of cardiovascular disease (CVD). Obesity is primarily considered to be a disorder of energy balance, and it has recently been suggested that some forms of obesity are associated with chronic low-grade inflammation. The present paper focuses on the current status of our knowledge regarding chronic inflammation, a link between obesity and CVDs, including heart diseases, vascular disease and atherosclerosis. The paper discusses the methods of body fat evaluation in humans, the endocrinology and distribution of adipose tissue in the genders, the pathophysiology of obesity, the relationship among obesity, inflammation, and CVD, and the adipose tissue-derived cytokines known to affect inflammation. Due to space limitations, this paper focuses on C-reactive protein, serum amyloid A, leptin, adiponectin, resistin, visfatin, chemerin, omentin, vaspin, apelin, and retinol binding protein 4 as adipokines.

/pdf/inflammation-a-link-between-obesity-and-cardiovascular-2w9km2ka6h.pdf

Inflammation, a Link between Obesity and Cardiovascular Disease

This book provides a series of reviews about pathophysiology, treatment, and, especially, diagnostic testing of clinical syndromes of autonomie failure. The book is organized into sections about integration of sympathetic and parasympathetic function, progressive autonomie failure, and syndromes of autonomie failure. Even cursory examination of the table of contents reveals a lack of consensus about the proper classification for the several conditions involving autonomie failure, reflecting our relative ignorance about pathophysiology in this new discipline in neurology. The chapter authors are well-chosen experts, the quality of writing is generally good, and the chapters fit together well. Several typographical errors are annoying or misleading (eg, description of prazosin as an ot-2 adrenoceptor blocker, page 164). The book is a worthwhile compilation for cardiologists, neurologists, endocrinologiste, and internists who evaluate patients with suspected autonomie failure and need to know the relevant diagnostic tests. Medical students, medical residents, and fellows should benefit from

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=intemed&articleId=605447&pdfFileName=archinte_145_3_006.pdf

Autonomic Failure: A Textbook of Clinical Disorders of the Autonomic Nervous System

Homocysteine (HMC) is a sulfur containing amino acid, which plays a role in methionine metabolism. Folic acid (FA) and vitamin B12 (B12) are essential for remethylization of HMC to methionine. HMC level increases in the deficiency of these vitamins. Hyperhomocysteinemia causes vascular endothelial damage, which causes atherosclerosis. The aim of this study is to investigate the effect of valproate (VA) and carbamazepine (CBZ) on the serum levels of HMC, B12, and FA.Thirty-six children receiving CBZ and 30 children receiving VA for epilepsy for the last 1-year period and 29 healthy children as control were the population of this study. After 6 h of fasting serum HMC, B12, and FA levels were measured and results were compared statistically. Mean values of HMC, FA, and B12 levels in control group were 9.2+/-2.7 micromol/l, 9.0+/-2.0 ng/ml, and 342+/-162 pg/ml, in VA group 14.0+/-6.8 micromol/l, 7.3+/-2.9 ng/ml, and 368+/-159 pg/ml, in CBZ group 16.0+/-13.1 micromol/l, 7.5+/-3.3 ng/ml, and 285+/-158 pg/ml, respectively. Serum HMC levels were higher in VA and CBZ groups than control group (P 0.05). In CBZ group serum B12 levels were lower than control group (P<0.05).FA may be added to the treatment protocol (if the patients take only CBZ, then B12 should also be added) for patients taking these antiepileptic drugs to decrease the degenerative effect of VA and CBZ on vascular endothelium.

Effects of valproate and carbamazepine on serum levels of homocysteine, vitamin B12, and folic acid.

Introduction: The aims of this study were to establish the prevalence of enuresis, to determine accompanying factors, and to identify common methods in the management of enuresis in

Enuresis prevalence and accompanying factors in schoolchildren: a questionnaire study from southeast Anatolia.

Childhood obesity is a complex syndrome, probably due to the multiplicity of contributing factors, contradictory literature information about etiology, prognosis, prevention and treatment. In the recent reports, autonomic nervous system (ANS) dysfunction has been documented in adult obesity. Autonomic nervous system functions in obese children are not clear. This study was planned to investigate autonomic nervous system function in childhood (7–13 years of age) obesity. Study and control groups consisted of 33 simple obese (23 boys and ten girls, mean age 9.5±1.4 years) and 30 healthy children (18 boys and 12 girls, mean age 10.1±1.8 years), respectively. Four non-invasive autonomic nervous system function tests (Orthostatic test, Valsalva ratio, 30/15 ratio, Heart rate responses to deep breathing) and general ophthalmic examination were performed on both groups. The difference between the obese and control groups was found statistically significant in Valsalva ratio, 30/15 ratio and Heart rate responses to deep breathing ( P P >0.05). Ophthalmic examinations were normal. The result of these tests suggested normal activity of sympathetic, and hypoactivity of parasympathetic nervous system, implying parasympathetic nervous system dysfunction as a risk factor or associated finding in childhood obesity.

Autonomic nervous system functions in obese children.

BACKGROUND The aim of this study was to investigate the relationships between plasma visfatin, insulin resistance, lipid profile and anthropometric measurements in obese children. SUBJECTS AND METHODS Plasma levels of visfatin, insulin, glucose, lipid profile and anthropometric indices were determined in 30 obese children and compared with those in 30 age- and gender-matched non-obese children. Visfatin was measured with enzyme-linked immunosorbent assay and logarithmically transformed to log visfatin for parametric comparisons. RESULTS The obese group had significantly elevated plasma visfatin, fasting glucose and insulin and homeostasis model assessment (HOMA) values, as well as elevated lipid concentrations, compared with non-obese children. In the obese group log visfatin correlated positively with weight (p = 0.007), waist circumference (p = 0.007), hip circumference (p = 0.034), BMI (p = 0.005), insulin (p = 0.041) and HOMA (p = 0.044). No correlation was found between visfatin and lipid profile in obese children (p >0.05). Linear regression analysis revealed significant positive relationships between log visfatin and BMI (p = 0.005), insulin and BMI (p <0.001), and between HOMA and BMI (p <0.001) in the obese group but not in the control group. Multivariate regression analysis with log visfatin as a dependent variable showed that only BMI (p = 0.005) and bodyweight (p = 0.014) correlated positively with log visfatin in obese children. CONCLUSIONS An increased visfatin concentration may be associated with BMI and insulin resistance in obese children. Although these findings may lay a foundation for further hypotheses, the limited sample size in the present study means that longitudinal studies with more patients are needed.

Plasma visfatin concentrations in childhood obesity: relationships with insulin resistance and anthropometric indices.

Background: Early detection of necrotizing enterocolitis can improve the prognosis, however, there is not a reliable laboratory test to detect either newborns at risk for necrotizing enterocolitis development or those at early stages of the disease. Since fecal lactoferrin and fecal calprotectin are inflammatory markers of gastrointestinal diseases, it was hypothesized that both these biomarkers could be successfully used in the diagnosis of necrotizing enterocolitis. Methods: In a prospective study, fecal lactoferrin and fecal calprotectin concentrations of 14 newborns with necrotizing enterocolitis and consecutively admitted 40 healthy preterm, and 23 healthy full-term newborns were measured with enzyme-linked immunosorbent assay technique. Results: Mean fecal lactoferrin and fecal calprotectin were not different between preterm and full-term newborns (p = .235 and p = .845, respectively), or those who were diagnosed with necrotizing enterocolitis or not (p = .545 and p = .968, respectively). Prevalence of necrotizing enterocolitis was 1.51% (14 of 2734). Stage of the disease did not have a statistical effect on mean levels (p = .694 and p = .267, respectively). Mean fecal lactoferrin and fecal calprotectin levels were not different in the case of breastfeeding (p = .623 and p = .792, respectively). Conclusion: Neither fecal lactoferrin nor fecal calprotectin has a role in the identification of necrotizing enterocolitis, especially in early stages of the disease. Further studies on wider necrotizing enterocolitis series are needed for a more definite conclusion.

Hamza Karabiber

Papers

Effects of valproate and carbamazepine on serum levels of homocysteine, vitamin B12, and folic acid.

Enuresis prevalence and accompanying factors in schoolchildren: a questionnaire study from southeast Anatolia.

Autonomic nervous system functions in obese children.

Plasma visfatin concentrations in childhood obesity: relationships with insulin resistance and anthropometric indices.

The role of fecal calprotectin and lactoferrin in the diagnosis of necrotizing enterocolitis