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Biomedical subjects

L Tamer

Publications and source records attributed to L Tamer.

28 records · Page 2Linked to original sources
PubMed2001

Serum L-carnitine levels and lipoprotein compositions in chronic viral hepatitis patients.

OBJECTIVES: The aim of this study was to evaluate the serum L-carnitine levels and its effect on lipoproteins in chronic viral hepatitis B or C patients. DESIGN AND METHODS: Blood samples were taken from 41 patients and 30 healthy subjects after 12 h fasting. RESULTS: Patients' serum L-carnitine levels (11.19 +/- 6.67 mg/L) (p < 0.0001) and hepatic enzyme activities (AST and ALT) (49.02 +/- 42.80 and 58.35 +/- 57.51 U/L) (p < 0.0005) were significantly higher than controls'. Serum total (3.85 +/- 0.82 mmol/L), LDL (2.08 +/- 0.76 mmol/L) and HDL (1.02 +/- 0.29 mmol/L) cholesterol levels were significantly lower in patients (p < 0.01). On the other hand triglyceride levels (1.65 +/- 0.85 mmol/L) were significantly higher in patients (p < 0.05). CONCLUSIONS: The higher L-carnitine levels of patients may result from the leakage of hepatic cellular carnitine. If there is a decreased hepatic cellular carnitine levels, this may affect the transport of acetyl moiety for cholesterol synthesis and alter lipoprotein composition. Further investigation is needed for hepatic tissue L-carnitine levels.

Adolescent↗
PubMed2001

Effect of anti-rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5'-triphosphatase and superoxide dismutase activation, and ultrastructural changes.

OBJECT: The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti-rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5'-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. METHODS: Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2-7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 microg) intraperitoneal injection of anti-rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. CONCLUSIONS: The results showed that neutralizing IL-6 bioactivity with anti-rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

Animals↗
PubMed1998

The effect of collagen, interleukin-1 alpha and glicosaminoglycan on the neovascularization of central nervous system.

Neovascularization, the development of a new microvasculature, has an important role in physiological and pathological processes. The vascular changes in the brain can be easily detected because the proliferation of endothelial cells in its vascular structure is quite small, and so constitutes a good model for neovascularization studies. In the present investigation, to induce intracerebral neovascularization, we implanted collagen, Interleukin-1 alpha (IL-1 alpha) and glicosaminoglycan into the brain of pigs, in order to test the hypothesis that IL-1 alpha, collagen and glicosaminoglycan play a pivotal role in the process of neovascularization. Both pure collagen and collagen combined with IL-1 alpha induced neovascularization according to light-electron microscopic findings and values of enzymes' activities. In particular, collagen combined with IL-1 alpha synergically affected the increase of neovascularization. However, glicosaminoglycan did not affect it significantly. Although the results of this study provided us with some interesting data indicating the beneficial effects of collagen combined with IL-1 alpha on neovascularization, further studies should be done to study the short term effect of these biochemical substances.

Adenosine Triphosphatases↗
PubMed1997

Serum copper, zinc and magnesium levels in children with enterobiosis.

Levels of serum copper (Cu), zinc (Zn) and magnesium (Mg) were determined in the sera of 250 children aged between 6 and 13. Of these children, 180 were infected only with Enterobius vermicularis. The remaining 70 children were without parasitic or bacterial infection and made up the control group. The cellophane tape method was used to detect E.vermicularis infection. The levels of Cu, Zn and Mg in the serum samples were measured with the Perkin- Elmer 2380 Atomic Absorption Spectrophotometer. Evaluation by the student-t test showed that the means of the Cu, Zn and Mg in the serum were significantly lower in the infected group than in the control group. Thus, in this study, we found that E. vermicularis adversely affects the level of elements such as Cu, Zn, and Mg in serum.

Adolescent↗
PubMed1996

Bencyclane as an anti-sickling agent.

A vasodilating Ca2+ channel blocker, bencyclane, was used in 18 patients with homozygous sickle cell anaemia (SCD) to test the possible anti-sickling effect. With bencyclane intervention the Na(+)-K+ ATPase activity increased from 256 +/- 29 to 331 +/- 37 nmol Pi/mg protein/h (P < 0.0001) and the Ca(2+)-Mg2+ ATPase level increased from 172 +/- 12 to 222 +/- 44 nmol Pi/mg protein/h (P < 0.0001). The intracytoplasmic Ca2+ concentration reduced from 3.5 +/- 0.6 to 2.7 +/- 0.25 mumol/l (P < 0.0001). The patient's blood contained fewer irreversibly sickled cells (ISCs) (a reduction from 21.4% to 14.4%) (P < 0.05). At the same time MCHC of the erythrocytes decreased from 34.5 to 33.0 g/dl (P < 0.05). Bencyclane appears to be a promising anti-sickling agent that can be used orally in SCD.

Adolescent↗
PubMed1994

Zinc, copper and magnesium status in insulin-dependent diabetes.

In 20 patients with insulin-dependent diabetes mellitus the concentration of zinc in serum was 56.53 +/- 2.36 micrograms/dl (mean +/- SD). This was significantly lower (p < 0.01) than the levels measured in matched controls. In the same patients the concentrations of serum copper and magnesium were 123.46 +/- 6.59 micrograms/dl and 17.38 +/- 0.52 mg/l respectively. These copper values were higher and the magnesium levels were lower than in the control subjects (p < 0.01). These changes may be associated with the development of insulin resistance and it is proposed that patients will improve if trace elements are given as part of the therapy.

Adolescent↗
PubMedDate not supplied

The relationship between leptin and lipids in atherosclerosis.

BACKGROUND: This study aimed to examine the extent to which leptin, alone or in combination with other risk factors, may be an independent marker for myocardial infarction in a region with a high incidence of cardiovascular disease. METHODS AND RESULTS: Leptin levels were measured by the ELISA method, while plasma lipids and lipoproteins were measured by conventional methods. Leptin levels were significantly higher in the patient than in the control group. Serum total cholesterol, low-density lipoprotein, lipoprotein (a) and apolipoprotein B showed a significant correlation with leptin, while high-density lipoprotein showed an inverse relation. CONCLUSIONS: Our results suggest that leptin may be one factor operating in the metabolic alteration taking place during myocardial infarction, and is a possible risk factor.

Apolipoproteins↗
PubMedDate not supplied

Apolipoprotein B gene polymorphisms in people in the east Mediterranean area of Turkey.

Point mutations in the receptor binding domain of low density lipoprotein may increase cholesterol levels in blood. Three mutations of Apo B-100 protein result in defective binding (Arg 3500 ----> [corrected] Gln, Arg 3500 ----> [corrected] Trp and Arg 3531 ----> [corrected] Cys). We estimated the frequency of Apo B point mutations (codon 3500) C9774T (Arg 3500 ----> [corrected] Trp) and G9775A (Arg 3500 ----> [corrected] Gln) in 179 atherosclerotic, 145 hyperlipidaemic individuals and 272 healthy individuals in the east Mediterranean region of Turkey. Lipid and lipoprotein levels were measured with routine biochemical analyser and Apo B mutation was detected using real-time PCR. Neither mutation was found. In this region, Apo B-100 protein mutations are rare and causes of hyperlipidaemia and atherosclerosis may therefore be unrelated to them.

Adult↗
PubMedDate not supplied

Glutathione S-transferase M1, T1, and P1 gene polymorphism in exudative age-related macular degeneration: a preliminary report.

PURPOSE: To elucidate whether the gene polymorphisms of glutathione S-transferase (GST) M1, T1, and P1 are associated with the development of exudative age-related macular degeneration. METHODS: The authors genotyped 35 white patients with exudative age-related macular degeneration and 159 healthy controls. Genomic DNA from peripheral blood was examined using polymerase chain reaction and defined for the genetic polymorphisms of GST. RESULTS: No association was observed between GSTM1, GSTT1, and GSTP1 polymorphisms and age-related macular degeneration risk (p>0.05). The frequencies of the combination of the GSTM1 (null) and GSTP1 (mutant), GSTM1 (null), and GSTT1 (null) genotype polymorphisms in patients with exudative age-related macular degeneration differed greatly from those of the control group (p=0.001 OR [95% CI]: 7.70 [2.28-25.98] and p=0.007 OR [95% CI]: 3.88 [1.51-10.02], respectively). CONCLUSIONS: The present study suggests that the GSTM1 (null) and GSTT1 (null), GSTM1 (null), and GSTP1 (mutant) combinations may be a genetic risk factor for the development of exudative age-related macular degeneration. However, the potential role of GST polymorphisms as a marker of susceptibility to age-related macular degeneration needs further studies in a larger number of patients.

Aged↗