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Biomedical subjects

M Tuncer

Publications and source records attributed to M Tuncer.

At least 55 records · Page 3Linked to original sources
PubMed2000

Dysplastic changes in idiopathic thrombocytopenic purpura and the effect of corticosteroids to increase dysplasia and cause hyperdiploid macropolycytes.

This study evaluates the dysplastic hematological changes in nine patients with idiopathic thrombocytopenic purpura (ITP) in 11 attacks, before and after corticosteroid treatment. The pretreatment blood smears of patients with ITP, displayed more neutrophils with bizarre nuclei (P < 0.001), Döhle or Döhle-like inclusions (P < 0. 01), irregular distribution of granules (P < 0.05), hypo-agranulation (P < 0.05), pseudo-Pelger-Huet-like cells (P < 0. 01), and nuclei with chromatine clumping (P < 0.01) than the normal children. The eosinophils of ITP patients were also dysplastic, before treatment. The pretreatment diameter of the neutrophils and the percentage of macropolycytes were greater than those of the patients with viral infections and normal group (P < 0.05 for all). The percentage of neutrophils with bizarre nuclei and nuclei with chromatine clumping and the diameter of neutrophils and macropolycyte percentage increased with corticosteroid therapy (P < 0.01, < 0.01, < 0.01, and < 0.05, respectively). The neutrophil diameter, percentage of macropolycytes, and number of neutrophils with bizarre nuclei decreased within 1-4 weeks after the therapy was stopped. In the neutrophils of two patients, diploidy and hyperdiploidy were established before and on the last day of therapy, respectively, and diploidy reversed after therapy was stopped. In conclusion, ITP patients display dysplastic findings in both neutrophils and eosinophils before treatment and corticosteroids cause transient significant increase in some of the dysplastic changes in neutrophils.

Adolescent↗
PubMed2000

Does serotonin relax the rat anococcygeus muscle via 5-HT7 receptors?

The mechanisms of serotonin (5-HT)-induced contraction and relaxation were studied in the rat anococcygeus muscle. In the presence of prazosin (1 nM) and ketanserin (10 nM), concentration/response curves to 5-HT were shifted to the right and the maximum effects were not affected (pKB values 9.09+/-0.29 and 8.66+/-0.06 for prazosin and ketanserin, respectively). On contrary, guanethidine (10 microM) antagonised the 5-HT-induced contractions non-competitively. In the presence of guanethidine, prazosin or ketanserin further inhibited the responses to 5-HT at lower concentrations. The serotonergic receptor agonists 5-carboxamidotrypamine, metoclopramide and sumatriptan did not produce any effect in tissues under baseline conditions. 5-HT caused concentration-dependent relaxation in phenylephrine (1 microM) -precontracted preparations in the presence of guanethidine (10 microM). Tetrodotoxin (1 microM), N(G)-nitro-L-arginine (100 microM) and capsaicin (1 microM) were ineffective in antagonising the relaxation induced by 5-HT. The serotonergic receptor antagonists: ketanserin (0.1 microM), ICS 205930 (10 microM), GR 113808 (10 microM), GR 55562 (10 microM), methiothepin (10 nM), mesulergine (10 microM), ritanserin (0.1 microM) and spiperon (0.1 microM) did not antagonise 5-HT-induced relaxation. On the other hand, clozapine (0.01-0.1 microM) and metergoline (0.1-1 microM) attenuated the relaxation induced by 5-HT. These results demonstrate that 5-HT contracts rat anococcygeus muscle directly by an action on alpha1-adrenergic receptors and indirectly by releasing noradrenaline from adrenergic nerve endings. None of the 5-HT receptors plays a role in the 5-HT-induced contractions. Moreover 5-HT induces concentration-dependent relaxation in the precontracted preparations which apparently are not mediated through known 5-HT receptor types.

Adrenergic alpha-Agonists↗
PubMed2000

A potential role for arginase in recurrent infections and hypertrophy of tonsillar and adenoidal tissue.

Since arginase has been found to be an arginine-depleting and nitric oxide synthase-regulating enzyme, the present study was devised to examine hypertrophied and infected tonsil and adenoid arginase activity in relation to a metabolic arginase-nitric oxide pathway and its association with disease processes. Tissues were taken from 32 children undergoing adenotonsillectomy. There was a statistically significant difference between the two tissue enzyme activities, with tonsillar arginase activity being higher than the corresponding adenoidal tissue (P < 0.005). This suggests a potential role for tissue arginase activity as an outcome module and a contributing factor in chronic recurrent infection and hypertrophy of tonsillar and adenoidal tissues.

Adenoids↗
PubMed2000

Factors responsible for acetylcholine-induced dilatation in the isolated perfused rat kidney.

Mechanism of acetylcholine (ACh)-induced dilatation was investigated in isolated perfused rat kidney. Under a constant flow of 8-10 ml/min, ACh (0.001-3 microg/0.1 ml) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine (PE). ACh-induced dilatations were inhibited by atropine (10(-6) mol/l), hexamethonium (10(-4) mol/l), indomethacin (10(-5) mol/l), methylene blue (10(-5) mol/l), N(G)-nitro-L-arginine (L-NOARG, 10(-4) mol/l), tetrodotoxin (TTX, 10(-6) mol/l), capsaicin (10(-6) mol/l), and glibenclamide (10(-5) mol/l). These results suggest that in the isolated perfused rat kidney, endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO), and tachykinin neuromediators may play a role in ACh-induced dilatation via stimulation of guanylate cyclase and opening of ATP-sensitive potassium channels.

Acetylcholine↗
PubMed2000

Chemical peritonitis associated with high dialysate acetaldehyde concentrations.

BACKGROUND: During the standard heat sterilization process of lactate-buffered peritoneal dialysis (PD) solutions, glucose degrades to form compounds called glucose degradation products such as acetaldehyde, formaldehyde, or glyoxal. Despite evidence that these products may be responsible for some in vitro cytotoxic effects induced by commercially available PD fluids, data on their acute or chronic effects on the human peritoneum is scarce. SUBJECTS AND METHODS: This case presentation is based on an observation of 21 aseptic peritonitis cases of unknown aetiology. All cases appeared within one month in a university hospital PD unit that had a peritonitis rate of 1 episode/26 patient months and 55 active patients on CAPD. Acetaldehyde level in the bags was assayed by gas chromatography. RESULTS: Twenty-one patients presented with signs of peritonitis including cloudy dialysate and abdominal tenderness with additional abdominal pain in 11 patients and vomiting in one. In all cases, cultures and Gram stains were negative for micro-organisms. Fever was not observed in any patient. Average dialysate white blood cell count was 1795/mm(3). All patients were free of intraperitoneal medication when symptoms appeared. Patients were using PD solutions from a newly established domestic production plant. Apparently all patients with symptoms of peritonitis used bags with the same lot number and the solution in the bags appeared to be darker in colour than that in bags with other lot numbers. Chemical analysis of the unused PD solution samples revealed acetaldehyde levels of 17-20 p.p. m. in bags containing darker solution, which is very high compared with the usual acetaldehyde level of 6 p.p.m. in heat-sterilized PD solutions. CONCLUSIONS: Based on the above findings, we hypothesize that higher levels of acetaldehyde and possibly other glucose degradation products may have been an aetiological factor in these 21 cases of chemical peritonitis. Our observation suggests that acetaldehyde, in concentrations 3-4 times higher than the usual level in commercially available PD solutions, may induce acute sterile peritonitis in CAPD patients.

Acetaldehyde↗
PubMed2000

[Gastritis localization and GERD incidence in patients with Cag A(+) and Cag A(-) Helicobacter pylori infection].

The relationship between Helicobacter pylori (HP) and gastroesophageal reflux disease (GERD) is very complex and still not well understood. However, many issues, even those as basic as whether HP induces or protects against GERD, are still controversial. The gastritis location could play also a role in the induction of GERD. Some investigators suggested that infection by the Cag A strain of HP seems to have a positive association with reflux esophagitis. Therefore, the aim of this study was to investigate the relationship between GERD, gastritis location, HP infection and Cag A positivity.

Adolescent↗
PubMed1999

Human MLH1 deficiency predisposes to hematological malignancy and neurofibromatosis type 1.

Heterozygous germ-line mutations in the DNA mismatch repair genes lead to hereditary nonpolyposis colorectal cancer. The disease susceptibility of individuals who constitutionally lack both wild-type alleles is unknown. We have identified three offspring in a hereditary nonpolyposis colorectal cancer family who developed hematological malignancy at a very early age, and at least two of them displayed signs of neurofibromatosis type 1 (NF1). DNA sequence analysis and allele-specific amplification in two siblings revealed a homozygous MLH1 mutation (C676T-->Arg226Stop). Thus, a homozygous germ-line MLH1 mutation and consequent mismatch repair deficiency results in a mutator phenotype characterized by leukemia and/or lymphoma associated with neurofibromatosis type 1.

Adaptor Proteins, Signal Transducing↗
PubMed1999

The relaxation induced by nicotine in the rat isolated renal artery.

The mechanism of nicotine-induced relaxation was investigated in the rat isolated renal artery. Nicotine (10(-3) M) produced a relaxation when preparations were precontracted by phenylephrine (3 x 10(-6) M). Nicotine-induced relaxation was 27.3 +/- 2.5% of phenylephrine contraction and was not affected by atropine (10(-5) M), guanethidine (10(-5) M), hexamethonium (10(-4) M), indomethacin (10(-5) M), N(G)-nitro-L-arginine (10(-4) M), methylene blue (10(-5) M), glibenclamide (10(-5) M), quinacrine (3 x 10(-6) M), tetrodotoxin (10(-6) M), capsaicin (10(-6) M), tetraethylammonium (10(-3) M), 4-aminopyridine (10(-3) M), and ouabain (10(-6) M) (n = 6, Mann-Whitney U-test). A calcium antagonizing effect of nicotine was not observed. Therefore, it appears that nicotine relaxes rat isolated renal artery by a nonspecific action on the vascular smooth muscle.

Animals↗
PubMed1999

Cyclosporine A preparations and their vehicles induce contraction of the guinea pig gallbladder in vitro: the role of cyclooxygenase metabolites.

The aim of this study was to establish whether prostanoids play a role in the contraction induced by cyclosporine A (CyA) preparations in the guinea pig isolated gallbladder strips. It was also aimed to study the effects of the preparations and their solvents on the acetylcholine-evoked rhythmic contractions of the guinea pig isolated sphincter of Oddi (SO). Isometric contractions were recorded. CyA parenteral and oral preparations and their vehicles, Cremophor-EL and Labrafil caused concentration-dependent and sustained contractions (74.2 +/- 6.2, 58.4 +/- 6.3, 88.9 +/- 4.9 and 47.5 +/- 6.2% of maximum KCl contraction, respectively) of gallbladder strips, but not of SO. Quinacrine, indometacin and ridogrel inhibited the contraction induced by CyA preparations and their vehicles in gallbladder strips (for CyA parenteral preparation, 34.7 +/- 6.7, 1.4 +/- 0.9, 19.0 +/- 6.4% of maximum KCl contraction, respectively). The drug and its vehicles changed neither the initial contraction nor the amplitude and frequency of the phasic contractions induced by acetylcholine in SO preparations. The results indicate that the drug is able to contract the gallbladder strips and the vehicles contribute to the contracting effect of CyA. Prostanoids may be responsible for the CyA-induced contraction of the gallbladder.

Acetylcholine↗
PubMed1999

Differentiation of leukemic cells induced by short-course high-dose methylprednisolone in children with different subtypes of acute myeloblastic leukemia.

Differentiation of myeloid leukemic cells to mature granulocytes by high-dose methylprednisolone (HDMP, 20-30 mg/kg/day) with a favorable antileukemic effect has previously been demonstrated in children with acute promyelocytic leukemia and acute myeloblastic leukemia (AML) M4. In the present study, three children with other morphological subtypes of AML (two AML M1, one AML M2) were given methylprednisolone (30 mg/kg/day) orally in a single dose. After a short-course (3 or 7 days) of HDMP treatment alone, a striking decrease in blast cells associated with an increase in maturing and abnormally nucleated polymorphonuclear-like cells some containing Auer rods were detected in all patients in peripheral blood or bone marrow smears. During HDMP treatment, in parallel to morphological improvements, marked increases in the percentage of cells expressing granulocytic antigen (CD15) were observed. The increase of CD15 expression on myeloid cells, together with the steady expression of CD34 and CD117 antigens in Casel(AML M1) , is suggestive of aberrant CD34 + CD117 + CD15 + cells, which may indicate the leukemic origin of the maturing myeloid cells. These results suggest that HDMP treatment may induce differentiation of myeloid leukemic cells in some children with different morphological subtypes of AML, and that the differentiation-inducing effect of HDMP should be explored in other malignant diseases.

Administration, Oral↗