• Clinical and Experimental Pediatrics
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• v.46 no.10
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• pp.966-971
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• 2003

Purpose : It is now well established that infection and inflammation play an important role in the pathogenesis of ischemic brain damage. The loss of neutrophils from systemic circulation is an associated finding in injury mediated by granulocyte. Periventricular leukomalacia(PVL) caused by ischemia is the principal form of brain injury in premature infants. This study was conducted to evaluate whether the low neutrophil count is associated with periventricular leukomalacia(PVL) in premature infants. Methods : Retrospective review of medical records was undertaken. Subjects were premature infants with a birth weight of less than 1,500 gm, admitted to the Neonatal Intensive Care Unit of Kyungpook University Hospital. A complete blood count of peripheral blood was done within the 1st hour of life. Neutropenia was defined as absolute neutrophil count < $1,500/mm^3$, PVL as increased periventricular echodensities followed by cyst formation on ultrasonography or corresponding signs on brain MRI. Results : Thirteen infants out of a total population of 37 revealed neutropenia. Respiratory distress syndrome and requirement for respiratory support were not different between infants with neutropenia( neutropenia group) and infants without neutropenia(control group). Intraventricular hemorrhage (IVH) and grade 3 and 4 IVH were more frequent in neutropenia group(P<0.05). There was no statistically significant increase of PVL in neutropenia group. The neutrophil count was $18,760.0{\pm}10,266.1/mm^3$, $7,272.0{\pm}7,435.0/mm^3$ infants with PVL and $11,131.7{\pm}3,386.5/mm^3$, $2,407.5{\pm}1,933.1/mm^3$ in infants without PVL, respectively. The frequency of mechanical ventilation and artificial surfactant therapy was higher in infants with PVL compared with infants without PVL, but statistical analysis was not performed due to small number of subjects. Conclusion : A low number of neutrophils in the systemic circulation was not associated with an increased risk of PVL in premature infants.

• Journal of Chest Surgery
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• v.43 no.6
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• pp.648-654
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• 2010

Background: This study assessed the early results of endovascular repair of acute type B aortic dissection and the aortic wall changes following endovascular repair. Material and Method: From July 2008 to May 2009, the preoperative and follow-up computed tomography (CT) scans of 5 patients with acute type B aortic dissection were evaluated, and these patients had underwent stent graft implantation within 13 days of the onset of dissection (mean: 7 days; range: 3~13). The whole lumen (WL), true lumen (TL) and false lumen (FL) diameters were measured at the proximal (p), middle (m) and distal (d) third of the descending thoracic aorta. Result: The study included four men and one woman with an average age of $59.4{\pm}20.1$ years (age range: 37~79 years). The follow-up CT was performed and evaluated at 7 days and 6 months. The primary tear was completely sealed in all the patients. No paraplegia, paresis or peripheral ischemia occurred and none of the patients died. No endoleaks developed in any of the patients during follow-up. The TL diameters increased from 20.4 to 33.5 mm in the proximal third (p/3), from 19.5 to 29.8 mm in the middle third (m/3) and from 15.2 to 23.5 mm in the distal third (d/3). The FL diameters decreased from 18.7 to 0 mm in the p/3, from 15.4 to 0 mm in the m/3 and from 21.4 to 8.7 mm in the d/3. The changes in the TL diameter were statistically significant in the middle and distal aorta, and those changes in the FL diameter were not statistically significant. There was a decrease in the WL after repair, but this was not statistically Significant. In three patients, the false lumen disappeared completely on follow-up CT at 6 months. Two patients had patent false lumens and no thrombosis. Conclusion: The early results showed that endovascular repair was effective in treating acute type B aortic dissection, and endovascular repair promoted positive aortic wall changes.

• Journal of Genetic Medicine
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• v.6 no.2
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• pp.155-160
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• 2009

Purpose: Preeclampsia is a multisystem human pregnancy-specific disorder. The pathophysiology of preeclampsia is linked with over-stimulation of inflammatory cytokines by placental ischemia via reduced uterine perfusion pressure during pregnancy. Although an increase in tumor necrosis factor (TNF)-alpha has been reported in preeclamptic women, there is little evidence of a relationship between TNF-alpha gene variations and preeclampsia. In this study, we identified a single-nucleotide polymorphism (SNP), C-850T, in the TNF-alpha gene promoter region in Korean preeclamptic women and investigated the association between this SNP and the development of preeclampsia. Materials and Methods: This polymorphism was analyzed in peripheral blood samples from 198 preeclamptic pregnancies and 194 normotensive pregnancies using a SNapShot kit and an ABI Prism 3100 Genetic analyzer. Results: Genotypes and allele frequencies for C-850T did not differ between preeclamptic and normotensive pregnancies. The distributions of genotypes (CC, CT and TT) were 74.3%, 22.2% and 3.5%, respectively, in preeclamptic pregnancies, and 71.6%, 25.8% and 2.6%, respectively, in normotensive pregnancies. The frequencies of the C and T alleles were 0.85 and 0.15 in preeclamptic pregnancies and 0.84 and 0.16 in normotensive pregnancies, respectively. There was no increased risk of preeclampsia in subjects with the CT (OR, 0.83; P=0.44) or TT genotypes (OR, 1.32; P=0.64). Conclusion: We found no differences in the genotypes or allele frequencies of the TNF-alpha gene polymorphism between preeclamptic and normotensive pregnancies. This study suggests that the TNF-alpha gene polymorphism may be not associated with the development of preeclampsia in pregnant Korean women.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.317-326
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• 1999

Background: Neural control of airway function is through parasympathetic, sympathetic and non-adrenergic, non-cholinergic mechanisms. The autonomic nervous system controls the airway smooth muscle tone, mucociliary system, permeability and blood flow in the bronchial circulation and release of mediators from the mast cells and other inflammatory cells. The cardiovascular and respiratory autonomic efferent fibers have a common central origin, so altered cardiovascular autonomic reflexes could reflect the altered respiratory autonomic status. Therefore, we performed this study to assess the autonomic abnormality and determine the correlating factors of severity of autonomic neuropathy in patients with chronic obstructive pulmonary disease(COPD) using easily reproducible cardiovascular autonomic reflex function test. Method: The study included 20 patients with COPD and 20 healthy persons obtained on Health Promotion Center in Yeungnam university hospital. All the patients had history and clinical features of COPD as defined by the American Thoracic Society. Any patients with myocardial ischemia, cardiac arrythmia, hypertension, central or peripheral nervous system disease, diabetes mellitus, or any other diseases known to produce autonomic neuropathy, has excluded. The autonomic nervous system function tests included three tests evaluating the parasympathetic system and two tests evaluating the sympathetic system. And also all subjects were subjected to pulmonary function test and arterial blood gas analysis. Results: Autonomic dysfunction was more commonly associated with patients with COPD than healthy person The parasympathetic dysfunction was frequent in patient with COPD, but sympathetic dysfunction seemed preserved. The severity of parasympathetic dysfunction in patients with COPD was correlated with the degree of duration of disease, smoking, reductions in the value of $FEV_1$ and FVC, and arterial hypoxemia but no such correlation existed for age, type of COPD, $FEV_1$/FVC, or $PaCO_s$. Conclusion: There is high frequency of parasympathetic dysfunction associated with COPD and the parasympathetic abnormality in COPD is increased in proportion to severity of airway disease. In COPD, parasympathetic dysfunction probably does not the cause of disease, but it may be an effect of disease progression.