Equity analysis audit of access and utilisation of Special Care Dental Services by ethnicity and social demographic markers.

OBJECTIVE: To identify and investigate any differences in utilisation of the, Sussex Community NHSFT, Special Care Dental Service (SCDS) across multiple demographic factors, including ethnicity, socio-economic groups and age in the Crawley area. METHOD: Data were audited for all new patients seen at the Crawley Special Care Dental Centre from November 2020-October 2021. Demographic data were compared to population data from the 2011 Census. Deprivation data, using Index of Multiple Deprivation, were also examined against utilisation and failure to attend appointments. RESULTS: A total of 1250 new patients accessed the Crawley SCDS between November 2020 and October 2021. The data suggests good equity to the service being utilised by the local community; the proportions of patients utilising the service over the course of a year from different ethnic groups reflected the demographic profile of Crawley. The proportion of failed appointments showed no correlation with deprivation decile. There was also no association between ethnic group and proportion of failed appointments. CONCLUSION: Ensuring equal utilisation of healthcare for all population groups has become a priority for healthcare providers. This audit found minimal inequities in utilisation of the Special Care Dental Service at Crawley.

How Approprıate are the Lengths of Syringe Needles Used for Subcutaneous Injections to the Children at School Age?

ABSTRACT Objectives: To define the normal ranges of the thicknesses of the skin and subcutaneous tissues via ultrasonography, and determine whether the current syringe needle-lengths used for the subcutaneous injections were appropriate. Methods: The thicknesses of the skin and subcutaneous tissues of 2244 students were measured at the left arm using ultrasonography. The patients were divided into three groups based on their age: 6-8, 9-12 and 13-17 years. Results: The thicknesses of the skin, subcutaneous tissue and skin-subcutaneous tissue were found to be positively correlated with their age, body mass index (BMI) and body surface area. All these were observed to be gender related. There was the possibility to make intramuscular injections for 50%, 25% and 25% of boys within the age groups of 6-8, 9-12 and 13-17 years, respectively. For girls, the risk of intramuscular injection was 25% for all the age groups. Conclusion: The study showed that the skin and skin-subcutaneous tissue thicknesses varied as a function of the patients' age, gender, BMIs and body surface areas.

Immediate adverse reactions to intravenous immunoglobulin in children: a single center experience.

Intravenous immunoglobulin (IVIG) is commonly used in primary and secondary immunodeficiency diseases as well as autoimmune conditions as immunomodulatator treatment. Immediate adverse events which are generally mild and occur during infusion are seen in 6 hours. Reported immediate adverse events are in a wide range from 1%-40% in pediatric patients. 115 patients who received IVIG (except newborns) were included into this crosssectional study. IVIG was given to patients for primary immunodeficiencies (n=8), ITP (n=65), Kawasaki disease (n=11), secondary immunosupression (n=28), and passive immunization (n=3). 5%, 10% IVIG preparations and pentaglobin were used. Headache, fever, chills, nausea, rash, arthralgia, myalgia and back pain were accepted as mild immediate events. There were 62 (54%) boys and 53 (46%) girls aged 1 month-18 years. Mean age of the group was 7.4±4.6 years. Immediate adverse events due to IVIG infusions were seen in 29 (25.2%) of all patients. Gender and types of the disease were not different in significance regarding the presence of adverse events. The rate of adverse events did not change with receiving pre-medication. The most common reaction was fever/chills. Immediate reactions were seen in first 6 hours in 7 patients and during infusion in the remaining. They were treated with slowing of the infusion rate and infusion was stopped in 3 patients because of moderate events. Because of the increasingly use of IVIG therapy, it is important to know the side effects. High doses, high infusion rates, accompanying infection may worsen the adverse effects especially in primary immunodeficiency diseases.

[The physical chemical and biological features of triglycerides. The cell absorption of functionally different palmitic+oleic lipoproteins of very low and density and linoleic+linolenic lipoproteins of low density.]

The earlier insulin-independent low-density lipoproteins and more late insulin-dependent very low-density lipoproteins implement different functions at the stages of phylogenesis. The disorder of biological function of trophology, alteration of fatty acids in triglycerides, prevalence of palmitic very low-density lipoproteins over oleic very low-density lipoproteins supply mitochondria of cells with non-optimal substrate - palmitic saturated fatty acid for gaining energy, ATP synthesis. Physiologically, cells implement oleic alternative of fatty acids metabolism, oxidizing mainly ω-9 endogenous oleic mono-unsaturated fatty acid. The pathology of low density lipoproteins is primary deficiency of poly-unsaturated fatty acids in cells, atherosclerosis and atheromotosis of intima of arteries of elastic type with development of dense plaques from poly-unsaturated fatty acids in the form of polyethers of cholesterol. The pathology of very low-density lipoproteins includes: a) syndrome of resistance to insulin; b) pathology of phylogenetically earlier insulin-independent visceral fatty tissue - metabolic syndrome; c) pathology of phylogenetically later insulin-dependent subcutaneous adipocytes - obesity; d) secondary atherosclerosis, under cumulation of palmitic low-density lipoproteins in blood with development of atherothrombosis of intima of arteries, soft plaques rich with triglycerides. As for the prevention of disorders of transfer of fatty acids to very low-density lipoproteins and low-density lipoproteins is common in many ways - minimization of aphysiological effect of surplus amount of food, biological function of diet. The prevention at the level of population includes: a) maximal limitation of content of palmitic saturated fatty acid in food; b) moderate increasing of polysaturated fatty acids, ω-3 poly-saturated fatty acids predominantly; c) increasing of physical activity. The pharmaceuticals are not provided by biology in primary prevention of metabolic pandemics under aphysiological impact of environment factors.

Active surveillance or radical prostatectomy? Which treatment is best?

OBJECTIVE: We evaluated the patients who are candidates for active surveillance and treated with radical prostatectomy. These patients were compared with other patients who had not met the criteria of active surveillance. METHODS: In total, 135 patients were included in the study. The patients were divided into two groups. The patients in Group 1 had less than three positive cores, Gleason 6 (3 + 3) and PSA level equal to or less than 10 ng/ml. Patients in Group 2 had three or more positive cores, Gleason 6 (3 + 3) and PSA level equal to or higher than 10 ng/ml. Pathological results of each groups were compared. RESULTS: The patients' ages were between 52 and 76, and 50 and 77 in groups 1 and 2, retrospectively. There were 69 and 66 patients in groups 1 and 2, retrospectively. The mean age of patients, PSA levels, PSA density, and prostate volumes were 63.89 ± 5.89 years, 5.82 ± 1.84 ng/ml, 0.14 ± 0.07 and 51.21 ± 31.75 cc (Group 1) and 65.77 ± 6.36 years, 13.65 ± 17.11 ng/ml, 0.63 ± 1.03 and 45.44 ± 26.77 cc (Group 2). T2a, T2c, T3a and T3b were reported in 28 patients, 36 patients, 3 patients and 2 patients after pathological evaluation in Group 1,respectively. T2a, T2c, T3a and T3b were reported in 13 patients, 47 patients, 5 patients and 1 patient in the other group, respectively. CONCLUSION: The final pathology showed that there is no difference in the positive surgical margin, proportion of insignificant prostate cancer and Gleason upgrading between groups. The clinicians must be aware of the fact that active surveillance can be misdiagnosed in some patients (Tab. 2, Ref. 20).

Plasma amino acid profile in autism spectrum disorder (ASD).

OBJECTIVE: In our study, we aimed to reveal pathophysiologic mechanisms in ASD by comparing plasma amino acid levels between patients and healthy controls while considering vitamin B12 and D levels. PATIENTS AND METHODS: The study included 21 patients aged 2-18 years-old who were followed with a diagnosis autism spectrum disorder (ASD) and 21 age and sex-matched healthy children from our outpatient clinic as control group. RESULTS: The study included 42 children and adolescents aged 2-18 years-old (19 girls and 23 boys). There were no significant differences in terms of body weight and height between the groups. We found significant differences in levels of ammonium, phosphoethanolamine, histidine, homocysteine, carnosine, methionine, cystathionine, cystine, threonine, 3-methyl histidine and phenylalanine/tyrosine ratio between patient and control groups. Both vitamin B12 and D were significantly lower in the ASD group compared to controls. In the variance analysis with vitamin B12 and D as covariates, significant differences persisted for only phosphoethanolamine (p=0.04), cystathionine (p<0.001), cystine (p=0.006) and threonine (p=0.02). CONCLUSIONS: Further studies are needed on the amino acids that show variations in children with ASD in order to reveal their role in the etiology and therapeutic use in ASD.

[THE LIPOLYSIS IN PHYLOGENETICALLY EARLY LIPOPROTEINS OF LOW DENSITY AND MORE LATER LIPOPROTEINS OF VERY LOW DENSITY: FUNCTION AND DIAGNOSTIC VALUE OF APOE AND APOC-III].

According to phylogenetic theory of general pathology, the function of low density lipoproteins (LDL) and hydrolysis of triglycerides (TG) in them under the effect of hepatic glycerol hydrolase apoC-III (HGH) developed at much earlier stages of phylogenesis than functioning of insulin-dependent phylogenetically late very low density lipoproteins (VLDL). For millions ofyears, lipolysis and HGH+apoC-III have activated transfer of polyenic fatty acids (FA) in the form of cholesteryl polyesters (CLE) from high density lipoproteins (HDL) to linoleic and linolenic LDL under the effect of cholesteryl ester transfer protein. It is reasonable to suggest that hepatocytes physiologically secrete oleic and palmitic VLDL and linoleic and linolenic LDL. Cells uptake ligand oleic and palmitic VLVL by apoE/B-100 receptor-mediated endocytosis. Physiologically, VLDL are not converted to LDL. If hepatocytes secrete palmitic VLDL in greater amounts than oleic VLDL upon slow hydrolysis ofpalmitic TG and under the effect of postheparinic lipoprotein lipase+apoC-II, only some proportion of palmitic TG is uptaken by cells as VLDL, and the rest is converted in ligand-free palmitic LDL These LDL increase plasma contents of TG and LDL-cholesterol and form small dense palmitic LDL. Expression of HGH+apoC-III synthesis compensates TG hydrolysis in nonphysiological palmitic LDL. In vivo, apoC-III is neither physiological no pathological inhibitor of lipolysis. Increase in plasma apoC-III content is an indicator of accumulation of non-physiological palmitic LDL and atherosclerosis-atheromatosis risk factor ApoE content ofpalmitic LDL increases together with apoC-III, i.e., apoE in ligand VLDL is not internalized via apoE/B-100 endocytosis. An increase in apoC-III and apoE contents are reliable in vivo tests for the rise inpalmitic FA, palmitic TG and excessive secretion of palmitic VLDL by hepatocytes. ApoC-III and apoE contents in LDL are additional tests to evaluate the efficiency of atherosclerosis prevention when physiological function of trophology and biological reaction of exotrophy are normalized.

Role of circulating nesfatin-1 in the underweight children with poor appetite.

OBJECTIVE: To investigate serum concentration of nesfatin-1 in underweight children who have poor appetite, and its association with anthropometric markers of malnutrition. PATIENTS AND METHODS: We recruited 50 underweight children and adolescents (aged 2-18 years) who presented with loss of appetite. Thirty age- and sex-matched controls were also included in the study. Fasting serum nesfatin-1 concentrations were measured by using Enzyme-Linked Immunosorbent Assay (ELISA) technique. RESULTS: Mean nesfatin-1 level was significantly higher in underweight children when compared to controls (p<0.001). There was no correlation between serum nesfatin-1 levels and anthropometrics markers. CONCLUSIONS: Our results suggest that nesfatin-1 might have an important role in regulation of food intake and pathogenesis of loss of appetite in children.

MEGALENCEPHALY, POLYMICROGYRIA, POLYDACTYLY AND HYDROCEPHALUS (MPPH) SYNDROME: A NEW CASE WITH OCCIPITAL ENCEPHALOCELE AND CLEFT PALATE.

The megalencephaly, polymicrogyria, polydactyly, and hydrocephalus (MPPH) syndrome is quite rarely seen. The four main findings in this syndrome may be accompanied by severe psychomotor retardation, blindness, hypotonia, convulsions, and facial dysmorphism. In this paper, we present a female newborn at 39 weeks gestational age born to parents who are first degree cousins. Beside the facial dysmorphism and four main features of the MPPH syndrome, the findings on the physical examination of the patient were, hypertonicity, occipital encephalocele, cleft palate, and multiple polyps in the tongue. The presence of occipital encephalocele, cleft palate, and polyps in the tongue in this patient was not reported previously in the literature.

[The fatty acids in blood plasma and erythrocytes in test of glucose tolerance].

The sample of 26 patients with ischemic heart disease and syndrome of insulin resistance was subjected to standard test of glucose tolerance. The content of individual fatty acids was detected using technique of gas chromatography and mass spectrometry. In blood plasma, after 2 hours of post-prandial hyperglycemia, reliably decreased content of C 16:1 of palmitoleic mono fatty acid, C 18:1 oleic mono fatty acid and in a lesser degree C 18:2 linoleic unsaturated fatty acid (p < 0.05). The level C 14:0 of myristic unsaturated fatty acid, C 16:0 of palmitic unsaturated fatty acid and with 18:0 of stearic unsaturated fatty acid, ratio C 16:0/C 16:1 and C 18:0/C 18:1 had no changes: content of both (omega-6 C 20:3 digomo-gamma-linoleic unsaturated fatty acid and essential polyenoic fatty acids remained the same. The significant differences between initial content in blood plasma of palmitic saturated fatty acid and oleic monoenic fatty acid was noted. The alteration in content of fatty acids in membranes of erythrocytes is the most expressed. In erythrocytes reliable (p < or = 0.05) decrease of content of C 16:0 palmitic fatty acid, C 18:0 stearic fatty acid and C 18:1 oleic fatty acid is established. The reliable decrease is noted in content of linoleic unsaturated fatty acid. In erythrocytes, moderate decrease is detected in levels of C 20:4 arachidonic polyenoic fatty acid, C 20:5 eicosapentaenoic polyenoic fatty acid. It is assumed that under post-prandial hyperglycemia insulin regulates metabolism of fatty acids, blocks lipolysis, decreases in cytosol of cells content of oleic and palmitic fatty acids inform of acetyl-KoA and forces mitochondrions intensively oxidate acetyl-KoA formed from pyruvate, from GLU. On surface of membrane, insulin increases number of glucose carriers GLUT4. Hypoglycemic effect of insulin is mediated by regulation first of all of metabolism of fatty acids. Hyperglycemia and insulin are two phylogenetically different humoral regulators. Insulin initiates blockade of lipolysis in adipocytes and positioning on membrane GLUT4. Hyperglycemia passively (activated) increases absorption by cells GLU on gradient of concentration inter-cellular medium--cytosol and synthesis of glycogen.

A male newborn with Simpson-Golabi-Behmel syndrome, presenting with metopic synostosis, anal atresia, and total anomalous pulmonary venous return.

Simpson-Golabi-Behmel syndrome is a clinical condition described by Simpson, characterized with multiple congenital anomalies and caused by Glypican 3 (GPC3) mutations of the X-linked gene. Typical findings such as overgrowth, hypoplastic changes of hands and feet, visceromegaly, cleft palate and macrocephalic distinctive facial features and multiple organ anomalies might be observed. GPC3 mutation is claimed to generally cause metopic synostosis. This case was reported because even though a lot of anomalies accompanying Simpson-Golabi-Behmel syndrome had been noticed, combination of metopic synostosis, has not been reported before.

[Low and very low density lipoproteins: pathogenetic and clinical significance].

LDLP and VLDLP have different biological functions: phylogenetically older LDLP transfer FA that serve as substrates for intracellular production of energy and ATP while VLDLP transfer FA--precursors of cell membranes and eicosanoids. The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. VLDLP consist of palmitic and oleic VLDLP and LDLP of linoleic and linolenic LDLP. The contribution of LDLP to the development of HLP atherosclerosis and atheromatosis is negligible. LDLP form palmitic and oleic VLDLP with hydrated LDLP density. Blockade of LDLP absorption by apoB endocytosis and deficit of poly-FA constitute the etiological basis of atherosclerosis. Its pathogenetic basis is the excess of palmitic VLDLP with LDPL density in the intercellular space that block absorption of linoleic LDLP with all transferred SC poly-FA. Atheromatosis is clinically and prognostically most significant symptom of atherosclerosis associated with accumulation of ligand-free VLDLP and LDLP in arterial intima of the elastic type as the local pool of interstitial tissue for intravascular pool of intercellular medium. Type 2 diabetes mellitus in aged patients is a symptom of atherosclerosis resulting from SC poly-FA deficit and GLUT4 incompetence. Insulin-dependent cells differ in the degree of insulin resistance. Non-alcoholic fatty liver disease, synthesis of a physiological palmitic TG by hepatocytes and excessive formation of palmitic VLDLP in liver integrate pathogenesis of atherosclerosis and hepatic steatosis. The main pathogenetic factor is the excess of palmitic s-FA and palmitic TG.

A study on the effects of pica and iron-deficiency anemia on oxidative stress, antioxidant capacity and trace elements.

Pica is defined as developmentally inappropriate consumption of nonnutritive substances for at least 1 month. There are a few studies on serum trace element levels of patients with pica. The literature contains contracting data on the levels of oxidative stress and antioxidant levels in patients with iron-deficiency anemia (IDA). The effect of pica on oxidative stress and antioxidant capacity has not been investigated yet. The present study evaluated the effects of pica and IDA on oxidative stress and antioxidant capacity as well as on the levels of trace elements including serum zinc and selenium in 47 children with IDA plus pica, 22 children with IDA only and 21 nonanemic children as controls. The results demonstrated significantly lower levels of serum selenium and zinc in pica and IDA groups compared to the control group. Total oxidant levels were highest in the pica group and consistently, the lowest total antioxidant capacity was observed again in the pica group. Comparison of pica and IDA groups yielded significantly lower levels of total antioxidant levels and significantly higher oxidative stress index in the pica group. Consequently, it is thought that the detrimental effects of pica within the organism were mediated by adverse impacts on antioxidant capacity and oxidative stress. These effects should be kept in mind while managing patients with pica.

[Diagnostic significance of different apolipoprotein levels during hypertriglyceridemia].

Active receptor-mediated uptake of fatty acids (as lipids in VLDLP and LDLP) involves dynamic apolipoproteins apoE and apoC-III. Modern methods allow apoB-100 and apoA-1 to be determined both separately and together in HDLP and VLDLP+LDLP. We estimated diagnostic significance of simultaneous apoE and apoC-III determination in the serum and two LP classes in the patients having either physiological levels of triglycerides or moderate and pronounced hypertriglyceridemia. Serum apoE and apoC-III increased with increasing triglyceride levels and percent of prebeta-LP fractions in electrophoresis. There was significant correlation between apoE and apoC-II content in the sera and in apoB-100 LP. It precludes using measurements of apoproteins for differential assessment of VLDLP and LDLP uptake by the cells or differential diagnostics of primary phenotypes and secondary hyperlipoproteinemias. The apoE content in LDLP was increased only in 1/5 of the patients with marked hyertriglyceridemia. The ApoE an apoC-III content in lipoproteins is of no diagnostic value; it is enough to determine serum apoprotein levels. Significant correlation between HDLP cholesterol and apoA-1 and between LDLP and apoB-100 questions the necessity of measuring serum apoA-1 and apoB.

[Lipoprotein-associated phospholipase A2 in subjects at low and moderate risk estimated by the SCORE scale].

The aim of the work was to elucidate the relationship between PLA2 content and results of the tests of abnormal lipid transfer in lipoproteins (LP) in subjects at low and moderate risk estimated by the SCORE scale. Another aim was to estimate the diagnostic value of plasma PLA2 content that was determined in 378 subjects (285 women and 93 men) aged 30-64 yr at low and moderate risk (SCORE scale). The patients were divided into groups depending on the age, the number of atheroscleroic plaques (ACP) in carotid arteries (0ACP 1 ACP, more than 1 ACP), enhanced and normal PLA2 levels. PLA2 was measured using PLAC Test Elisa Kits (DiaDexus, USA), with the upper normal limit assumed to be 200 ng/ml. In women, PLA2 levels positively correlated with apoA-1 (main HDLP apoprotein) content (r = 0.51, p < 0.03); in men, PLA2 negatively correlated with TG (r = -0.38, p < 0.01); in subjects with homogeneous ACP PLA2 positively correlated with LP(a) (r = -.38, p < 0.03). Simultaneous rise in PLA2 and LP(a) levels may be a significant risk factor of atherosclerosis and atherothromhosis. Enhanced levels of TG, PLA2, and LP(a) may be the biochemical triad of "soft" plaque formation in the intima.

[The subcellular organelles of peroxisome, realization of biologic functions of trophology, homeostasis, endoecology and functional bond with mitochondrion: the lecture].

The biologic role of peroxisomes in cells is that the organelles in respect to fatty acids, lipids and substrates synthesized from acetate implement the same fimnctions as the lysosomes exercise to proteins and polypeptides. The biologic role of peroxisomes is to optimize in vivo the exogenous fatty acids in hepatocytes under the realization of biologic functions of trophology, homeostasis, endoecology. About 800 individual fatty acids can penetrate into organism with food. At that, no more than thirty of them undergo the metabolic transformation in vivo. The rest hundreds of fatty acids are aphysiologic and have to be oxidized into peroxisomes under isochronic activation of alpha-, beta- and omega-oxydases without ATP formation. If in peroxisomes are formed fatty acids that can oxidize mitochondrions by beta-oxidation then the proteins of cytosol transfer fatty acids from peroxisomes to mitochondrions. The mitochondrions oxidize fatty acids in the Krebs cycle to form ATP. The oxidation in peroxisomes concerns the fatty acids with odd numbers of carbon atoms, the transforms of unsaturated fatty acids, the very long chain fatty acids, the fatty acids with carbon atoms side-chains, the dicarboxylic fatty acids, the fatty acids with benzene or indole rings in carbon atoms chains. The peroxisomes oxidize the surplus amount of exogenous palmitic saturated fatty acid too. The peroxisomes implement the biologic.function of endoecology on autocrine level supporting the "purity" of cells cytosol and interact functionally with mitochondrions. In the intercellular medium of paracrine cells coens the fimctions of endoecology are realized by the Toll-similar receptors by the "our-not our" principle concerning phospholipids, positional aphysiologic triglycerides and proteolipids. In the peroxisomes, under the simultaneous oxidation of very long chain fatty acids, the synthesis by primate cells is possible of some amount of essential unsaturated and polyene fatty acids. The limited formation by animal cells of glucose from fatty acids is possible in the sequence "acetoneacetol spirit-metilglyoxal-D-glucose. The mutations in primary structure of peroxisomes oxidases are the main in-herent pathology.

[The individual fatty acids in blood plasma, erythrocytes and lipoproteins. The comparison of tests results of patients with ischemic heart disease and volunteers].

According to the generally accepted theory, the atherosclerosis is a kind of disorder of metabolism of lipids which chemically are the ethers of fatty lipids with spirits. Hence, the atherosclerosis is fatty acids pathology. In conformity with the biologic classification, among fatty acids it is functionally valid to distinguish saturated fatty acids without double bonds; monoenic fatty acids with one double bond; unsaturated fatty acids with two or three double bonds and polyenic fatty acids with four of six double bonds in chain. The saturated and monenic fatty acids are the substrates for cells to groundwork energy, ATP The unsaturated fatty acids in vivo are needed to form membranes. The polyenic fatty acids are essential since they are precursors of cell synthesis of humoral regulators--eicosanoids (prostanoids and leukotrienes). To clarify the pathogenesis of the "metabolic pandemics" most prevalent in human population, the quantitative determination of individual fatty acids in blood plasma and erythrocytes using gas chromatography technique is needed. It is necessary to evaluate the content of medium chain fatty acids; palmitic and stearic saturated fatty acids; oleic monoenic fatty acid and its transforms--linoleic, linolenic and dihomo-gamma-linolenic unsaturated fatty acids; essential polyenic omega-6 arachidonic, omega-3 eicosapentaenoic and docosahexaenoic fatty acids. The higher is in food the content of palmitic saturated fatty acid, palmitoleic and trans-vaccenic monoenic fatty acids, the more is in patient diet of beef meat and products of fat cow's milk. The higher is ratio of palmitic/oleic fatty acids the lower is the risk of formation of atheromatosis of arteries intima and development of ischemic heart disease and vice versa. The decrease of ratio of omega-3/omega-6 essential polyenic fatty acids is undesirable in prognostic sense. The metabolism of these acids differs and functional activity of omega-3 eicosanoid type 3 is higher In case of deficiency of omega-3 and omega-6 polyenic fatty acids in cells eicosanoids are synthesized from unsaturated dihomogamma-linolenic fatty acid and their influence turns out to be aphysiologic. This condition is a pathogenic foundation of atherosclerosis. There is a diagnostic reason to detect fatty acids in case of diabetes mellitus, obesity, metabolic syndrome and partially arterial hypertension.

CD4- and CD3-T lymphocyte reference values of immunocompetent urban and rural subjects in an African nation.

Studies on the reference values of CD4 and CD3 T cells in healthy individuals have continued to gain significance because of the importance of these immunological markers in the initiation of combination antiretroviral therapy (cART). The aim of the present study was to determine and compare the reference values of CD4 and CD3 T cells in urban and rural Nigerians who were human immunodeficiency virus (HIV), hepatitis B virus (HBV) and hepatitis C virus (HCV) negative. After ethical clearance and informed consent, 1123 subjects who met the inclusion criteria [mean age = 24.4 (± 11.2) years] were recruited in this study. Blood samples were analysed using the BD FACScount cytometer according to the manufacturer's instructions. Of the overall 1123 subjects, reference means of CD4, CD3 and CD4/CD3 ratio were 1030 ± 367, 1757 ± 609 cells/µl and 0.59 ± 0.08, respectively. Five hundred and fifty-one (49.1%) were an urban population with the mean CD4, CD3 and CD4/CD3 T cell ratio of 1032 ± 369, 1761 ± 612 cells/µl and 0.59 (±0.08), respectively. The remaining 572 (50.9%) were of a rural population with the mean CD4, CD3 and CD4/CD3 T cell ratio of 1028 ± 459, 1753 ± 958 cells/µl and 0.59 ± 0.13, respectively. Subjects with higher CD4 and CD3 T cells were more likely to be female than male (P < 0.05). There was no significant difference between the T cell values of the two populations (P > 0.05). Our findings provide new insight in the CD4 and CD3 T cell reference values of Nigerians.

[The secretory phospholipase A2 and transport of lipids by lipoproteins in patients with the risk of cardio-vascular pathology (the system "score") of lower and average degree. The diagnostic significance of the test].

The clinical and pathomorphologic data demonstrate that the most frequent cause of cardiac infarction is the formation of "soft" atheromatosis plaques in the intima of arteries. Their rupture results in thrombosis of coronary arteries. The plaques are characterized by higher content of triglycerides. On the basis of the research data, it is possible to validly consider that the detection of secretary phospholipase content A2 conjugated with lipoproteins is the test of systemic inflammatory response. This response is formed under atherosclerosis in vivo as a feedback to the accumulation in the intercellular medium of the endogenic flogogens (initiators of biological reaction of inflammation)--lipoproteins of lower density subclass A. Their utilization in the intima, as a pool of local interstitial tissue, by the resident macrophagocytes transformed from monocytes result in the formation of doth soft and disposed to laceration atheromatosis plaques and the atherothrombosis of coronary arteries and rarer of carotids. Concurrently, the increase of lipoproteins content in blood plasma is supposed to be the test of proliferation of cells in vivo, the smooth muscle cells of medium in particular. The simultaneous detection of content of secretory associated with lipoproteins phospholipase A2 and lipoprotein (a) can be considered as a valid risk factor of atherosclerosis and atherothrombosis--atheromatosis of intima of arteries with the formation of "soft" plaques in the intima, their laceration and thrombosis of coronary arteries and clinical presentation of cardiac infarction. The diagnostic triad of formation of soft plaques in the intima can be composed of the higher level of triglycerides, the content of protein of phospholipase A2 and lipoprotein (a).

[The unity of pathogenesis of insulin resistance syndrome and non-alcoholic fatty disease of liver. The metabolic disorder of fatty acids and triglycerides].

The pathogenesis of non-alcoholic fatty disease of liver (steatosis) is still as unclear as a loss of hepatocytes similar to apoptosis, development of biological reaction of inflammation, its transformation into steatohepatitis with subsequent fibrosis and formation of atrophic cirrhosis. The article suggests that steatosis is developed due to higher concentration of palmitic saturated fatty acid (C 16:0) in food, intensification of its endogenic synthesis from food carbohydrates and glucose and development of insulin resistance. It is displayed in in hormone ability to activate both oxidation in cells of glucose and synthesis of oleic monoene fatty acid from palmitic saturated fatty acid (C 18:1). The insulin resistance initiates pathologic process on the level of paracrine associations of cells resulting in permanent increase of concentration of non-etherified fatty acids in intercellular medium and intensification of their passive absorption by cells. The phylogenetically ancient mitochondrions will not to oxidize glucose until non-etherified fatty acids are present in cytosol and hence there is an opportunity to oxidize them. To eliminate undesirable action of polar saturated palmitic fatty acid, the cells etherify it by spirit glyceride into triglycerides to deposit in cytosol or to secrete into blood in a form of lipoproteins of very low density. Under insulin resistance, saturated palmitic fatty acid synthesized by hepatocytes from glucose, does not further transform into oleic monoenic fatty acid. The cells are to etherify endogenic (exogenic) palmnitic saturated fatty acid into composition of aphysiologic palmitic triglycerides (saturated palmitic fatty acid in position sn-2 of spirit glyceride). At that, triglycerides of palmitat-palmitat-oleat and even tripalmitat type are formed. The melting temperature of tripalmitat is 48 degrees C and melting temperature of physiologic trioletat is 13 degrees C. The intracellular lipases factually can't hydrolyze palmitic triglycerides. So, hepatocytes, overloaded by them, are destroyed in a way similar to apoptosis. The formed corpuscles of apoptosis disorder the biologic function of endoecology and trigger biologic reaction of inflammation. At that, steatosis changes into steato-hepatitis. The prevention of steatosis consists in dramatic restriction of concentration of palmitic saturated fatty acid in food. The treatment effect is targeted to: decreasing the formation of palmitine triglycerides by force of concurrent etherification of palmitic saturated fatty acid not into triglycerides but into phosphatidylcholine (symmetric phospholipids of soya); intensification of oxidation of palmitic saturated fatty acid in peroxisomes (glytazones and fibrates); decrease of insulin resistance (binuanide metformine).