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A Szczepanik

Publications and source records attributed to A Szczepanik.

At least 19 recordsLinked to original sources

Spread of a single multiresistant methicillin-resistant Staphylococcus aureus clone carrying a variant of staphylococcal cassette chromosome mec type III isolated in a university hospital.

The purpose of the study was the molecular characterization of methicillin-resistant Staphylococcus aureus (MRSA) isolates cultured from patients treated in seven wards of a university hospital in Lublin, Poland, over a 14-month period. Eleven nosocomial MRSA isolates were analyzed. Phenotypic identification of the isolates as MRSA was confirmed by the detection of the nuc and mecA genes using a multiplex PCR assay. The MRSA isolates were further characterized by pulsed-field gel electrophoresis, 16S-23S rRNA spacer length polymorphism analysis, and the simplex and multiplex SCCmec PCR assays. The MRSA isolates were found to be multiresistant: in addition to resistance to beta-lactam agents, they demonstrated resistance to ciprofloxacin, tetracycline, erythromycin, and gentamicin. The MRSA isolates were genetically identical and shared common pulsed-field gel electrophoresis profiles and 16S-23S rRNA spacer length polymorphism profiles. The PCR-based method revealed that the profile of the Lublin clone was identical to that of the Brazilian pandemic MRSA isolates. By SCCmec typing, all MRSA isolates harbored the C variant of the SCCmec type III that differed from the typical SCCmec type III pattern by the lack of locus F (414 bp). The results of this study indicate the spread of a single, multiresistant, MRSA clone in various wards of a university hospital over a 14-month period. The SCCmec structure harbored by the Lublin clone has previously been identified among Polish MRSA isolates representing the HoMRSA-Pol1 clone. The data from this study indicate that the Lublin MRSA clone is most probably genetically related to the HoMRSA-Pol1 clone. Moreover, this latter clone belongs to ST239, the same sequence type as the Hungarian and Brazilian pandemic MRSA isolates.

Bacterial Proteins↗

Dipyridamole inhibits hydroxylamine augmented nitric oxide (NO) production by activated polymorphonuclear neutrophils through an adenosine-independent mechanism.

Polymorphonuclear neutrophils (PMN) are thought to play a role in reperfusion injury and ischemia. These effects are partly mediated by toxic oxygen species (superoxide anion, hydrogen peroxide and hydroxyl radical) acting at the level of the endothelium. It was demonstrated recently that the superoxide anion reacts with nitric oxide (NO) and that interaction leads to the generation of highly toxic peroxynitrite. Several drugs were tested so far in order to affect PMN function. It was demonstrated that dipyridamole (2,6-bis-diethanolamino-4,8-dipiperidinopyrimido-(5,4-d)-pyrimidine) can influence neutrophil function by inhibiting adenosine uptake. However, this action can not fully explain all of the observed effects of dipyridamole action on PMN metabolism. The aim of our study was to evaluate the influence of dipyridamole on nitric oxide production by activated polymorphonuclear neutrophils. Incubation of PMNs with hydroxylamine (HA) and phorbol myristate acetate (PMA) generated nitrite (36.4+/-4.2 nmol/h 2x10(6) PMN), dipyridamole at 100 micromol/l, 50 micromol/l and 10 micromol/l caused a considerable drop in nitrite production (11.8+/-1.8, 19.7+/-2.7 and 27.4+/-3.2 nmol/h, respectively). Neither adenosine nor the adenosine analogue could mimic the dipyridamole effect. Moreover theophylline, an adenosine inhibitor could not reverse the dipirydamole action on PMN metabolism. We also found that dipyridamole inhibited hydrogen peroxide release from neutrophils. Catalase that scavenges hydrogen peroxide also largely abolished nitric oxide release from PMN. It is evident that dipyridamole inhibits hydroxylamine-augmented nitric oxide production by activated polymorphonuclear neutrophils through an adenosine-independent mechanism.

Adenosine↗

Prospective evaluation of hydroperoxide plasma levels and stable nitric oxide end products in patients subjected to angioplasty for coronary artery disease.

BACKGROUND: Oxidative stress appears to be involved in several processes that contribute to atherogenesis and restenosis following vascular intervention. METHODS: The aim of our study was to evaluate prospectively the plasma concentrations of a hydroperoxide (ROOH) and nitric oxide end product (NO(x)) in patients subjected to coronary angioplasty (PTCA) and routine control angiography 6 months after the initial procedure. We prospectively studied 48 consecutive patients (39 men, nine women, mean age 52 years) with stable angina who underwent successful elective angioplasty. A vascular segment was considered successfully treated when the residual luminal narrowing in the dilated segment immediately after angioplasty was <50%. Angiographic follow-up was obtained in all of the patients. Plasma samples were drawn at baseline (before angioplasty) and serially after angioplasty (1, 3 and 6 months afterwards). Hydroperoxides were determined by the FOX II assay (ferrous oxidation in xylenol orange, Pierce Rockford, IL). Nitrate was converted in the presence of NO3 reductase. The Griess reagent was used for the measurement of NO2. RESULTS: The overall angiographic restenosis rate was 35%. There were no significant differences in clinical variables between the patients with or without restenosis. The baseline levels (0.8+/-0.09 vs. 0.6+/-0.2 micromol/l) as well as the concentrations of authentic lipid hydroperoxide in plasma after 1 month (0.7+/-0.09 vs. 1.0+/-0.2 micromol/l) and 6 months (0.8+/-0.1 vs. 1.0+/-0.2 micromol/l) were similar in both groups. Three months after the angioplasty a significant increase in the ROOH level was noticed in the patients with restenosis (0.9+/-0.1 vs. 1.4+/-0.2, P=0.04). Plasma levels of NO(x) were similar in both groups at baseline (23.6+/-2.1 vs. 22.7+/-2.6 micromol/l) and 1 month after procedure (24.4+/-2.2 vs. 23.4+/-3.3 micromol/l). However, in patients with restenosis significant decreases in stable NO end products were observed 3 and 6 months after PTCA (18.1+/-1.5 vs. 13.3+/-1.7, P=0.04; 14.2+/-1.0 vs. 8.7+/-1.3, P=0.02, respectively). CONCLUSIONS: In patients with angiographic restenosis a significant increase in lipid peroxidation accompanied by a reduction in the stable end products of nitric oxide in plasma is observed several months after PTCA.

Angioplasty, Balloon, Coronary↗

Hydrogen peroxide and superoxide anion production by polymorphonuclear neutrophils in patients with chronic periapical granuloma, before and after surgical treatment.

Chronic periapical granuloma represents a localized tissue injury with well established signs of systemic immunological reactions. The aim of the study was to investigate changes in superoxide anion and hydrogen peroxide production by polymorphonuclear neutrophils (PMN) in patients with chronic periapical granuloma before and after surgical treatment. The affected teeth were extracted from 20 patients with chronic periapical lesions. Blood samples were obtained at admission, before extraction and on day 14. PMNs were isolated from blood samples and superoxide anion (O2-) and hydrogen peroxide (H2O2) production were estimated without stimulation and after stimulation of the cells with opsonized zymosan. Similar procedures were performed with blood samples obtained from 20 healthy controls. Superoxide anions as well as hydrogen peroxide production by unstimulated cells obtained from patients before treatment were significantly higher in comparison with controls. Fourteen days after extraction O2- production by unstimulated cells was higher than the controls and significantly lower in comparison to PMNs obtained before treatment, while H2O2 production was not significantly higher when compared to controls and significantly lower in comparison with PMNs obtained before extraction. The results obtained strongly imply the termination of a generalized inflammatory response after elimination of local inflammation by tooth extraction.

Adult↗

Energy metabolism in uncoupling protein 3 gene knockout mice.

Uncoupling protein 3 (UCP3) is a member of the mitochondrial anion carrier superfamily. Based upon its high homology with UCP1 and its restricted tissue distribution to skeletal muscle and brown adipose tissue, UCP3 has been suggested to play important roles in regulating energy expenditure, body weight, and thermoregulation. Other postulated roles for UCP3 include regulation of fatty acid metabolism, adaptive responses to acute exercise and starvation, and prevention of reactive oxygen species (ROS) formation. To address these questions, we have generated mice lacking UCP3 (UCP3 knockout (KO) mice). Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e. increased state 3/state 4 ratio), indicating that UCP3 has uncoupling activity. In addition, production of ROS is increased in mitochondria lacking UCP3. This study demonstrates that UCP3 has uncoupling activity and that its absence may lead to increased production of ROS. Despite these effects on mitochondrial function, UCP3 does not seem to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induced thermogenesis. The absence of such phenotypes in UCP3 KO mice could not be attributed to up-regulation of other UCP mRNAs. However, alternative compensatory mechanisms cannot be excluded. The consequence of increased mitochondrial coupling in UCP3 KO mice on metabolism and the possible role of yet unidentified compensatory mechanisms, remains to be determined.

Animals↗

The influence of treatment of hypercholesterolemic patients with simvastatin on plasma chemotactic activity and adherence of neutrophils.

BACKGROUND: there is some evidence to indicate that statins may affect the function of immune and inflammatory cells. This study investigates the influence of short term treatment with simvastatin on plasma chemotactic activity and adherence of polymorphonuclear neutrophils in hypercholesterolemic patients. METHODS AND RESULTS: 20 hypercholesterolemic patients (250-400 mg/dl) were given simvastatin (20 mg daily for 12 weeks). Peripheral blood samples were taken before and after 4 and 12 weeks of the therapy. The percentage of neutrophils adhering to plastic surface coated with albumin was significantly higher when cells were incubated with plasma obtained after 12 weeks of treatment with simvastatin in comparison with plasma collected before the therapy (unstimulated neutrophils: 5.945+/-0.475% vs. 8.155+/-0.96%, P=0.0477, stimulated neutrophils: 39.09+/-4.540% vs. 29.18+/-3.702%, P=0.032). There was a significant negative correlation between adherence of stimulated neutrophils and total cholesterol levels ((r)=-0.2796, 95% CI -0. 4999 to -0.02526, r(2)=0.07817, P=0.032). Migration of neutrophils towards plasma obtained after 12 weeks of treatment with simvastatin was significantly higher than towards plasma collected before the therapy (7.038+/-1.127 vs. 4.505+/-0 618 P=0.0475). CONCLUSION: treatment of hypercholesterolemic patients with simvastatin increases the chemotactic activity of plasma and augments the adherence of human neutrophils.

Anticholesteremic Agents↗

Plasma-mediated stimulation of neutrophil superoxide anion production during coronary artery bypass grafting: role of endothelin-1.

BACKGROUND: Activation of polymorphonuclear neutrophils (PMN) and subsequent release of free oxygen radicals, including the superoxide anion (O2-) has been shown to result in postischaemic myocardial dysfunction during coronary artery bypass grafting (CABG). Several neutrophil-oriented stimuli are known to be released from myocardium during ischaemia and reperfusion. Release of endothelin-1 has been documented during CABG. The aim of the current study was to evaluate plasma-mediated neutrophil stimulation and to verify whether endothelin-1, known to be a stimulus for PMN, is involved in plasma-mediated stimulation of PMN during coronary artery bypass grafting. METHODS: Plasma samples from peripheral artery, peripheral vein, and coronary sinus were obtained from 21 patients undergoing CABG before aortic clamping (global ischaemia), immediately after beginning reperfusion, and 30 min after reperfusion as well as from healthy controls. Plasma was incubated with PMN isolated from healthy donors preincubated in the presence of saline or specific endothelin-1 receptor antagonist (ET-A). PMN O2- production was measured spectrophotometrically. RESULTS: Plasma samples taken from the coronary sinus at the beginning of reperfusion were capable of higher stimulation of neutrophil superoxide anion production (24.2 +/- 2.0 nmol/5 x 10(6)PMN/30 min) than plasma obtained before reperfusion (15.6 +/- 1.5; p < 0.05) or plasma taken from peripheral artery (17.1 +/- 1.7; p < 0.05). Preincubation of PMN with endothelin-1 receptor antagonist decreased superoxide anion production by cells exposed to plasma taken from coronary sinus at the beginning of reperfusion (17.6 +/- 2.0, p < 0.05). CONCLUSIONS: Transcardiac release of soluble stimuli for PMN occurs as a result of myocardial ischaemia during CABG. Endothelin-1 may be involved in the plasma-mediated stimulation of neutrophil superoxide anion production.

Adult↗

Fibrinolytic therapy and n-acetylocysteine in the treatment of patients with acute myocardial infarction: its influence on authentic plasma hydroperoxide levels and polymorphonuclear neutrophil oxygen metabolism.

Recently it has been demonstrated that the administration of n-acetylocysteine (NAC), in combination with streptokinase, significantly diminished oxidative stress in patients with myocardial infarction. The aim of our study was to assess the influence of NAC treatment, as adjunct therapy in an evolving myocardial infarction, on the polymorphonuclear count, superoxide anion and hydrogen peroxide levels and nitric oxide production by PMNs and authentic plasma hydroperoxide (ROOH). Treatment of patients with NAC in addition to reperfusion therapy was accompanied by a significant decrease in the number of circulating polymorphonuclear neutrophils. However, the oxygen metabolism of PMNs was not affected by NAC administration. The concentration of authentic plasma hydroperoxide was significantly reduced by the administration of NAC which suggests diminished oxidative stress during acute myocardial infarction.

Acetylcysteine↗

[The quality of life after chemotherapy in advanced non-small cell lung cancer patients].

The intensity of complains, short survival and great number of patients makes many oncologists to apply chemotherapy in advanced non-small cell lung cancer/NSCLC/. The achieved median duration of life after chemotherapy was 6 to 12 month. From the other hand non small cell lung cancer chemotherapy is a big burden even to healthy persons. It can worsen the quality of life. That was the reason we evaluated the quality of life after chemotherapy in advanced non small cell lung cancer patients. Taking into account, that the evaluation of quality of life, used in most diseases is useless in advanced NSCLC patients, for appreciation the quality of life in these cases the lung cancer symptoms scale/LCSS/was adopted. In 110 non small cell lung cancer patients in stage IIIB and IV, who received combined chemotherapy by Le Chevalier/Vindesine, Cisplatin, Cyclophosphamide, Lomustin/or by Rosell/Mitomycin, Cyclophosphamide, Cisplatin/the quality of life was evaluated. In 20-persons control group all patients received the symptomatic treatment. In observed group of 110 patients, tumor regressions after 4 courses of chemotherapy allowed to resect cancer in 14 cases, to apply radiotherapy in 42 and to continue chemiotherapy in 23 persons. In every person from above mentioned group the quality of life was evaluated on the basis of intensity of cancer symptoms, accordingly to LCSS. The intensity of cancer symptoms was compared before and after treatment. There were compared; the innensity of complains, weakness, appetite, malnutrition, and hematological, neurological, performans state as well as respiratory sufficiency, infections, cardiac disorders and pain. Apart it, the side effects of applied therapy were assessed in 5 degree scale. The level of hemoglobin, the number of leucocytes, thrombocytes, bilirubine and transaminases in peripheral blood, hematurie, proteinurie, bleedings, appetite, nausea, vomitings, diarrhea, mucosal lesions, infections, skin lesions, cardiac lesions, neurological lesions, respiratory disorders, allergy, alopecia. It was established that, chemotherapy in the most patients improved the performance status and minimized cancer symptoms especially, after good response to treatment. After anticancer therapy more frequently severe infections and cardiac disorders, independently to results of treatment were seen. In non-responders, the cancer symptoms were intensified by side effects of antineoplastic-therapy. In this group of patients the severe side effects of therapy more frequently were seen.

Adult↗

[Assessment of plasma fibronectin concentration in type 1 diabetic patients].

Fibronectin is a family of glycoproteins that are present on many cell surfaces, in extracellular matrix and in plasma. Fibronectin might play an important role in pathogenesis of chronic diabetic complications. The aim of this study was to estimate plasma concentration of fibronectin in patients with recently onset and with long duration of type 1 diabetes mellitus. Moreover, the correlation between fibronectin concentration and HbA1c, duration of diabetes and late diabetic complications was assessed. The study was performed in 18 patients with recently onset of diabetes (aged 23.8 +/- 5.3 years, HbA1c 10.63 +/- 0.83%) (group A) and 21 patients with long history of diabetes (aged 33.9 +/- 10.5 years, mean diabetes duration 9.8 +/- 5.8 years, HbA1c 9.24 +/- 2.48%) (group B). The plasma concentration of fibronectin was estimated with the use of the ELISA test. The plasma fibronectin concentration was significantly higher in type 1 diabetic patients in comparison with healthy subjects (381.00 +/- 27.42 and 297.50 +/- 25.32 micrograms/ml, respectively, p < 0.05). The values observed in the patients with recently onset and long duration of diabetes and in the subjects with and without diabetic complications did not differ significantly (p > 0.05, p > 0.05). We noticed positive correlation between fibronectin concentration and HbA1c (r = 0.35; p < 0.05) and negative correlation with patients age (r = -0.35; p < 0.05). The results of our study suggest, that plasma fibronectin concentration in diabetes is increased independently from microangiopathy but rather results from hyperglycaemia.

Adult↗

Plasma chemotactic activity during dipyridamole induced myocardial ischemia.

BACKGROUND: We have previously reported that transient myocardial ischemia induced during exercise or dipyridamole challenge leads to the release of increased amounts of hydrogen peroxide into circulating blood. It would indicate that the temporary functional changes within myocardial cells may constitute there a sterile inflammatory area. Therefore we decided to evaluate the chemotactic properties of plasma in patients undergoing dipyridamole provocative test, as a sign of released inflammatory mediators. The ischemia occurrence was evaluated with 99mTc-SestaMIBI followed by single photon emission computed tomography (SPECT). METHODS: Blood samples were obtained from the peripheral vein of 42 patients (18 men and 24 women, mean age 61 years). Plasma chemotactic activity was determined by the use of the Boyden chamber method: immediately before dipyridamole challenge (time 0), 7, and 30 min after drug infusion. The migration of control polymorphonuclear neutrophils towards evaluated plasma samples was estimated. RESULTS: Chemotaxis of control PMNs towards plasma isolated from patients without signs of myocardial ischemia 7 min after dipyridamole administration was significantly diminished in comparison with baseline values (p=0.003). Plasma obtained 7 min after dipyridamole infusion from patients manifesting signs of myocardial ischemia by SPECT attracted control PMNs significantly more intensively in comparison to plasma isolated at time 0 (p=0.0005). CONCLUSIONS: The obtained results indicate that transient myocardial ischemia induced by dipyridamole challenge leads to generation of chemotactic factors detectable in peripheral blood plasma.

Angina Pectoris↗

Detection of cancer cells in the blood by FACS sorting of CD45- cells.

We describe a simple and sensitive method for detection of low number of cancer cells in the blood. The method is based on FACS sorting of leukocytes labelled with anti-CD45 monoclonal antibody and examining CD45- cells by conventional cytology and immunostaining for cytokeratin 18. In a model study, cancer cells seeded at the frequency of 1 per 106 and 1 per 107 leukocytes were detected in CD45- population. Sensitivity of this method was comparable to reverse transcription polymerase chain reaction (RT-PCR) used for detection of cancer cells expressing CD44 variants-mRNA. In a pilot study, cancer cells were also isolated from the blood of some patients with locally advanced gastric cancer. This method may be useful for detection of circulating tumour cells in cancer patients.

Blood Cells↗

Vancomycin down-regulates lipopolysaccharide-induced tumour necrosis factor alpha (TNF alpha) production and TNF alpha-mRNA accumulation in human blood monocytes.

The cytokines play an important role in the cascade of the pathological events leading to septic shock. The TNF alpha produced by monocytes/macrophages upon stimulation with bacterial fragments may contribute to induction of this cytokine cascade. Moreover, the antibiotics used for antimicrobial therapy may cause the increase of TNF alpha production due to massive bacterial killing and exposure of monocytes/macrophages to bacterial cell constituents. To investigate the effect of Vancomycin on TNF alpha production, an in vitro model of LPS-stimulated monocytes was used. The level of TNF alpha protein or TNF biological activity were tested in the culture supernatants of monocytes with LPS. Vancomycin down-regulated, in dose-dependent manner, the TNF alpha production. Vancomycin also inhibited TNF alpha-mRNA accumulation in LPS-stimulated monocytes, as assessed by fluorescence in situ hybridization (FISH) in cell suspension. The down-regulation of TNF alpha production in LPS-stimulated monocytes may indicate that inhibition of this cytokine release is one of the important therapeutic effects of Vancomycin in sepsis.

Animals↗

Effects of magnetic resonance imaging on polymorphonuclear neutrophil functions.

RATIONALE AND OBJECTIVES: Limited research has been performed on the effects of magnetic resonance (MR) imaging on the immune system. To our knowledge, there are no reported studies of MR imaging effects on the polymorphonuclear neutrophil (PMN) system. Therefore, we evaluated the influence of MR imaging exposure on PMNs. METHODS: In vivo and in vitro studies were performed on 36 patients undergoing MR imaging. The following were estimated in blood samples: leukocyte and PMN count, PMN phagocytosis and bactericidal capacity, percentage of cells with expression of surface receptor for the Fc fragment of immunoglobulin G (IgG), PMN superoxide, hydrogen peroxide production, and plasma lysozyme activity. Another sample of patients was used to eliminate temperature as an influence on changes in PMN functions. RESULTS: Both in vitro and in vivo MR imaging led to a decrease in PMNs and an increase in PMN phagocytosis, bactericidal capacity, hydrogen peroxide production, and percentage of cells with expression of surface receptor for Fc IgG. Superoxide anion production did not change significantly. Elevated temperature, stress, and anxiety were excluded as influences on our results. CONCLUSION: The PMN system is affected seriously by MR imaging.

Adolescent↗

Superoxide anion (O2-) production and bactericidal capacity of polymorphonuclear neutrophils obtained from patients subjected to glucagon test.

Superoxide anion (O2-) production and bactericidal capacity of morphologically mature bone marrow polymorphonuclear neutrophils (PMN) were evaluated in 30 haematologically normal individuals. These same parameters of peripheral PMNs were estimated in 15 healthy volunteers before and after glucagon-induced marrow granulocyte reserve mobilization. Bone marrow PMN in comparison with cells obtained from peripheral blood manifested impaired superoxide anion production and diminished bactericidal capacity. The admixture of bone marrow PMN released into the circulation by the use of glucagon administration significantly lowered both estimated PMN functions.

Adult↗

Characterization of human pancreatic adenocarcinoma cell line with high metastatic potential in SCID mice.

The CD44 molecule and CD44 isoforms are expressed on some malignant tumours and it has been suggested that their expression may correlate with tumour spread. Human pancreatic carcinoma cell line (HPC-4) expressing CD44 was established from a patient with adenocarcinoma of pancreas. This line showed a rapid growth in vitro, several chromosome abnormalities and surface expression of some adhesion molecules (ICAM-1, LFA-3, beta 1-chain of VLA integrins, VNR). Xenotransplanted HPC-4 cells were able to grow rapidly in SCID mice as subcutaneous tumour, leading to 100% mortality within 3-5 weeks when 1 x 10(5)-1 x 10(7) cells were inoculated. Spontaneous metastases in the liver, lung, spleen and kidney of SCID mice were observed. Interestingly enough, HPC-4 cells in vivo and ex vivo also expressed HLA-DR molecules, but these were rapidly lost upon culture in vitro. It is suggested that the appearance of HLA-DR may be the result of interaction of the tumour with a local environment of the host, while CD44 expression may explain the rapid growth and occurrence of distant metastases in SCID mice. The ability of HPC-4 cells to form spontaneous metastases in SCID mice may prove to be a potentially interesting model of human carcinoma for testing new treatment modalities.

Adenocarcinoma↗

[Clinical probes using tumor necrosis factor in treatment of neoplastic diseases].

Tumor necrosis factor-TNF is a cytokine that is predominantly produced by the activated macrophages. It was shown that TNF has the antineoplastic activity in vitro or in tumor xenografts on the animals in vivo. Clinical trials phase I and II carried out in many centers assessed toxic effects of TNF administration, as well as its pharmacokinetic and therapeutic effect. The following paper is a survey of the results of clinical trials which could be useful for the assessment of TNF role in oncological immunotherapy.

Animals↗

Impairment of the oxygen-dependent microbicidal mechanisms of polymorphonuclear neutrophils in patients with type 2 diabetes is not associated with increased susceptibility to infection.

Phagocytosis, bactericidal capacity and some selected parameters of oxygen-dependent bactericidal mechanisms were evaluated in 20 patients with type 2 diabetes being in similar (intermediate) state of metabolic control and in 15 healthy individuals. Polymorphonuclear neutrophils (PMNs) from diabetics showed normal ability to phagocytose staphylococci, a decreased Intracellular bacteria killing, the impaired stimulated superoxide anion (O2-) and hydrogen peroxide (H2O2) production and the low intracellular myeloperoxidase activity. The obtained data seem to indicate that the decreased bacterial killing by PMNs isolated from diabetics are partly at least related to an impairment of the oxygen-dependent bactericidal mechanisms. Since none of the diabetic patients suffered from recurrent infection the clinical significance of our finding is still uncertain.

Adult↗