• Applied Microscopy
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• v.5 no.1
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• pp.1-8
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• 1975

These studies were carried out the observation of polymorphonuclear leukocyte phagocytosis of Candida albicans in vitro and also detected to the cytoplasmic changes of polymorphonuclear leukocyte during phagocytosis by the method of electron microscopy. The results were summarized as follows: 1. In normal polymorphonuclear leukocyte, nuclear lobes showed a preponderance of dense, granular chromatin located peripherally. The cytoplasm of polymorphonuclear leukocyte was not extensive; the cytoplasmic matrix was moderate dense and of a granular appearance. Golgi complex and rough endoplasmic reticulum system was poorly developed. But a various type of granules were seen abundantly. 2. After 30 minutes of incubation, Candida albicans was completely engulfed. These had come to lie in the vacuole which was limited by the membrane. 3. After 90 minutes of incubation, the phagocytic vacuoles were larger, and many granules devoid of membranes were seen within them. Though the granules has lost their membrane after entering the vacuoles. 4. After 2 hours of incubation, the cytoplamsic components of polymorphonuclear leuko cytes were changed their original morphology.

• Restorative Dentistry and Endodontics
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• v.6 no.1
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• pp.71-75
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• 1980

The purpose of this study was to determine the close relation between clinical symptom and histopathologic finding in pulp. 20 samples of pulp tissue were collected from badly decayed teeth with considerable pulp vitality. Hemogram was also made with the first drop of bleedieg after total pulp extirpation (10cases) and vital pulpotomy(10cases). Histologic specimen was made routinely with extirpated pulp and stained by H&E and P.A.S. Stains. The results under microsopic examination were as follows; 1. Hemogram obtained from dental pulp with acute inflammation revealed increase of polymorphonuclear leukocyte in number, more lymphocytes and monocytes. 2. Hemogram from pulp with chronic inflammation shown the number of lymphocyte and monocyte was remarkably increased. 3. Histologi specimen obtained from teeth with severe clinical symptome showed polymorphonuclear leukocyte infiltration and the hemogram also showed polymorphonuclear leukocytes. 4. Specimen from teeth with moderate symptom showed lymphocyte infiltration and vessel dilatation underneath decayed area. Erythrocytes were massively accumulated inside of the vessel wall.

• Journal of Periodontal and Implant Science
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• v.14 no.1
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• pp.70.2-70.2
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• 1984

• Journal of Korean Neurosurgical Society
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• v.38 no.3
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• pp.221-226
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• 2005

Objective : Reactive oxygen metabolites and polymorphonuclear leukocytes have been implicated in the pathophysiology of reperfusion injury. The mechanisms involved in superoxide-mediated leukocyte adherence remain unclear, however, nitric oxide[NO] may contribute to this response. The present study is undertaken to elucidate mechamisms controlling NO based mechanisms that regulated leukocyte-endothelial interactions in the cerebral vasculature after global cerebral ischemia and reperfusion. Methods : Pial venular leukocyte adherence of anesthetized newborn piglets was quantified by in situ fluorescence videomicroscopy through closed cranial windows during basal conditions and during 2hours of reperfusion after global ischemia induced by 9minutes of asphyxia. Nitric oxide synthase[NOS] was inhibited by local window superfusion of L-nitroarginine[NA]; superfusion of sodium nitroprusside[SNP] was used to donate NO. Results : The mean number of adherent leukocytes to cerebral venules in the 9minutes asphyxia and 2hours reperfusion group were $161{\pm}19$ compared with $13{\pm}4$ in the nonasphyxial group. Superfusion of L-NA through the cranial window for 2hours resulted in leukocyte adherence similar to that observed during the initial 2hours of reperfusion after asphyxia. Leukocyte adherence was not additionally increased in asphyxic animal treated with L-NA. SNP inhibited asphyxia induced leukocyte adherence back to control levels. Conclusions : Nitric oxide inhibits leukocyte adherence to cerebral venules during the initial hours of reperfusion after asphyxia, and that NO supplementation inhibit asphyxia induced leukocyte adherence back to control levels. These results indicate that NO is an important factor in ischemia-reperfusion induced leukocyte adherence.

• The Korean Journal of Zoology
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• v.9 no.1
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• pp.16-20
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• 1966

The frequency of sex chromatin in neutrophil leukocyte of 14 female and 4 male normal, adult rabbits was examined and compared to those of single total X-ray irradiation. 1. The average frequency of of drumstck was 9 % in female and 0.1% in male, and that of sessile nodule was 3.35% in female and 0.9% in male , in normal condition rabbit . These results fairly determined sex ratio by sex chromatin in neutrophil leukocyte. 2. The drumstick frequency reduces to half after X-irradiaton but did not show any regular tendency or variation in morphologicla form, indicating the stability of chromatin to X-irradiation. 4. The chromatin satellite was found with a reasonable frequency in the some kinds of irradiated cells, polymorphonuclear neutrophil (above 7 lobes 0 and megakarycyte.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.319-327
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• 2004

This study was aimed at evaluating the effect of defibrotide on the development of the surgically induced reflux esophagitis, on gastric secretion, lipid peroxidation, polymorphonuclear leukocytes (PMNs) accumulation, polymorphonuclear leukocytes adherence, superoxide anion and hydrogen peroxide production in PMNs, scavenge of hydroxyl radical and hydrogen peroxide, cytokine (interleukin-1 ${\beta}$, tumor necrosis $factor-{\alpha}$) production in blood, and intracelluar calcium mobilization in PMNs. Defibrotide did not inhibit the gastric secretion and not change the gastric pH. Treatment of esophagitis rats with defibrotide inhibited lipid peroxidation, and myeloperoxidase (MPO) in the esophagus in comparison with untreated rats. Defibrotide significantly decreased the PMN adherence to superior mesenteric artery endothelium in a dose-dependent manner, Superoxide anion and hydrogen peroxide production in $1{\mu}M$ formylmethionylleucylphenylalanine (fMLP)- or $0.1{\mu}g/ml$ N-phorbol 12-myristate 13-acetate (PMA)-activated PMNs was inhibited by defibrotide in a dose-dependent fashion. Defibrotide effectively scavenged the hydrogen peroxide but did not scavenge the hydroxyl radical. Treatment of esophagitis rats with defibrotide inhibited interleukin-1 ${\beta}$ production in the blood in comparison with untreated rats, but tumor necrosis $factor-{\alpha}$ production was not affected by defibrotide. The fMLP-induced elevation of intracellular calcium in PMNs was inhibited by defibrotide. The results of this study suggest that defibrotide may have partly beneficial protective effects against reflux esophagitis by the inhibition lipid peroxidation, PMNs accumulation, PMNs adherence to endothelium, reactive oxygen species production in PMNs, inflammatory cytokine production(i.e. interleukin-1 ${\beta}$), and intracellular calcium mobilization in PMNs in rats.

• Journal of Periodontal and Implant Science
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• v.25 no.3
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• pp.733-740
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• 1995

This investigation was undertaken to determine the relationship between the amount of polymorphonuclear leukocyte(PMN) enzyme myeloperoxidase(MPO) in gingival crevicular fluid(GCF) collected from active or control site and gingival disease status described by clinical indices(gingival index, papillary bleeding index, pocket depth, periotron unit). The results were as follows : 1. MPO activity/site was greater at active sites than at control sites. 2. According to increasing the clinical parameters, MPO/sites was higher statistically (P<0. 01, P<0.05). 3. High MPO(unit/site) groups was higher statistically than low MPO(unit/site) groups in various clinical parameters. 4. Correlation coefficients between MPO(unit/site) and GI, MPO($unit/{\mu}l$ GCF) and periotron unit were 0.4782, -0.5901, respectively.

• Neonatal Medicine
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• v.24 no.1
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• pp.26-31
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• 2017

Purpose: To identify the factors associated with differential diagnosis of neonatal bacterial meningitis at the earliest opportunities possible and to evaluate the value of the bacterial meningitis score especially in neonates. Methods: We conducted a single-center, retrospective study of neonates diagnosed meningitis at our hospital between January 2000 and March 2014. We compared the general characteristics, clinical manifestations, laboratory findings, bacterial meningitis scores between the bacterial group and the aseptic group. Results: Bacterial meningitis differs significantly from aseptic meningitis in platelet count, the cerebrospinal fluid polymorphonuclear leukocyte count, and the serum protein including also the albumin (P<0.05). Except two infants, the bacterial meningitis score over 2 accurately predict bacterial meningitis in the other 11 infants. Conclusion: The bacterial meningitis score appears highly useful to identify neonatal infants with bacterial meningitis. However, its diagnostic and prognostic value is just 'adjunctive', because low score cannot rule out bacterial meningitis.

• Biomolecules & Therapeutics
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• v.1 no.2
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• pp.131-136
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• 1993

In the present study, the effect of $HgCl_2$on the function of human peripheral polymorphonuclear leukocytes(PMNs) was examined. PMNs were isolated from human peripheral blood with density centrifugation in Ficoll-Paque. The cells were then incubated with $0.5{\sim}5{\mu}M\;HgCl_2$and glass adherence, chemotactic activity and erythrocyte-antibody rosette forming activity were measured. $HgCl_2$ decreased the function of PMNs in all three aspects tested. $HgCl_2$significantly diminished glass adherence(40.5 {\mu}M: 92{\pm}12%$ (percentage of control, $mean{\pm}$ S.D.); 41 {\mu}M: 46{\pm}11%,$ P<0.01; $3{\mu}M: 35{\pm}7%,$P<0.01;$5{\mu}M:49{\pm}10%,$ P<0.01). Similarly, significant differences were observed in chemotactic activity after $HgCl_2$treatment compared with control (control: $0.95{\pm}0.14mm; 0.5 {\mu}M: 0.91{\pm}0.11 mm; 1 {\mu}M: 0.77{\pm}0.16mm, P<0.05; 3{\mu}M: 0.61{\pm} 0.06mm, P<0.01; 5{\mu}M: 0.15{\pm}0.03 mm, P<0.01).$ Also, 4HgCl_2$decreased the percentage of rosette-forming PMNs, indicating diminished phagocytic activity of PMNs upon $HgCl_2$ exposure compared with control (control: $58{\pm}4%; 1{\mu}M: 53{\pm}4%, p<0.05; 3{\mu}M: 49{\pm}3%, P<0.01; 5{\mu}M: 46{\pm}3%, P<0.01).$ Cell viability was not antered after $HgCl_2$treatment (483{\pm}5%$ viability in control PMNs versus $81{\pm}8%$ viability in $5{\mu}M$ Hg-treated PMNs), suggesting that the impaired PMN function after $HgCl_2$treatment was not due to nonspecific cytotoxicity induced by $HgCl_2$. $HgCl_2$-induced decrease in the function of PMNs may have some implications in depressed host susceptibilityupon bacterial challenge after mercury exposure.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.43-50
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• 2004

Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. Amrinone, a specific inhibitor of phosphodiesterase 3, has an antioxidant activity against PMNs. Therefore, we hypothesized that amrinone could attenuate PMNs-Induced cardiac dysfunction by suppression of reactive oxygen species (ROS) produced fby PMNs. In the present study, we examined the effects of amrinone on isolated ischemic (20 min) and reperfused (45 min) rat hearts perfused with PMNs. Amrinone at $25\;{\mu}M$, given to hearts during the first 5 min of reperfusion, significantly improved coronary flow, left ventricular developed pressure (P<0.001), and the maximal rate of development of left ventricular developed pressure (P<0.001), compared with ischemic/reperfused hearts perfused with PMNs in the absence of amrinone. In addition, amrinone significantly reduced myeloperoxidase activity by 50.8%, indicating decreased PMNs infiltration (p< 0.001). Superoxide radical and hydrogen peroxide production were also significantly reduced in fMLP- and PMA-stimulated PMNs pretreated with amrinone. Hydroxyl radical was scavenged by amrinone. fMLP-induced elevation of $[Ca^{2+}]_i$ was also inhibited by amrinone. These results provide evidence that amrinone can significantly attenuate PMN-induced cardiac contractile dysfunction in the ischemic/reperfused rat heart via attenuation of PMNs infiltration into the myocardium and suppression of ROS release by PMNs.