• The korean journal of orthodontics
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• v.24 no.1 s.44
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• pp.37-62
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• 1994

This study was undertaken to investigate the three dimensional vascular changes of periodontal ligament following orthodontic tooth movement. Experimental tooth movement was carried out in 96 Sprague-Dawley rats with the weight of 250g. They were divided into four experimental groups (each 24 rats). The left maxillary first molar was moved mesially with 25g force in group I, and with 75g force in group II. Each three animals were sacrificed after 1, 6, 12, 24 hours, and 3, 7, 14, 21 days. In group III, 25g mesial force was applied for 3 days, and in group IV, 75g mesial force was applied for 3 days. Then the appliances were removed, and each three animals were sacrificed after 1, 6, 12, 24 hours, and 3, 7, 14, 21 days from removal of appliance. The contralateral molars were used for control group. Casting media was injected via left ventricle and polymerized in warm water. After corrosion of surrounding soft tissue, three dimensional vascular changes were examined using scanning electron microscopy. The findings of this study were as follows: 1. Pressure side of group I and II showed degenerative vascular changes such as vascular compression, reduction of vasculature, leakage of casting media. But, regenerative changes were dominant after 7 days of tooth movement. Although the degenerative vascular changes were more severe in group II, which was exposed to heavy force, the timing of these changes was not different between two groups. 2. Periodontal vasculature was reestablished by the growth of new capillaries and their differentiation and union from the remaining periodontal vessels and vessels of alveolar bone marrow. Although vascular regeneration was more rapid in group I, which was exposed to light force, the vasculature was not fully normalized in both groups even after 21 days. 3. There was no remarkable changes in tension side of group I and II, but looping of capillary, new capillary growth, dilation of vessels, redirection of vessels in the direction of tensile force were occurred. 4. In pressure side of group III and IV, in which appliance was removed after 3 days of orthodontic force, bone resorption was continued even after removal of appliance. Regeneration of vasculature was initiated after 1-6 hours, and it was more rapid in group III than group IV. In both groups, the vasculature was not fully normalized even after 21 days. 5. After removal of appliance, tension side of group III and IV showed vascular compression and loss of vasculature.

• Annals of Surgical Treatment and Research
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• v.95 no.5
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• pp.278-285
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• 2018

Purpose: We investigated the clinical outcomes of deceased donor kidney transplantation (KT) using kidneys with terminal acute kidney injury (AKI). Methods: Between February 2000 and December 2013, we performed 202 deceased donor renal transplants from 159 brain dead donors. According to the expanded criteria donor (ECD) and AKI network criteria, we divided 202 recipients into 4 groups: Group I: Non-AKI & standard criteria donor (SCD) (n = 97); group II: Non-AKI & ECD (n = 15); group III: AKI & SCD (n = 52); and group IV: AKI & ECD (n = 38). Results: The incidence of delayed graft function (DFG) was significantly higher in patients with AKI than it was in the non-AKI group (P = 0.008). There were no significant differences among the 4 groups in graft survival (P = 0.074) or patient survival (P = 0.090). However, the long-term allograft survival rate was significantly lower in group IV than it was in other groups (P = 0.024). Conclusion: Allografts from deceased donors with terminal AKI had a higher incidence of DGF than did those from donors without AKI. However, there is no significant difference in graft and patient survival rates among the groups. So, the utilization of renal grafts from ECDs with terminal AKI is a feasible approach to address the critical organ shortage.

• Korean Journal of Radiology
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• v.22 no.3
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• pp.324-333
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• 2021

Objective: The clinical course of an individual patient with heart failure is unpredictable with left ventricle ejection fraction (LVEF) only. We aimed to evaluate the prognostic value of cardiac magnetic resonance (CMR)-derived myocardial fibrosis extent and to determine the cutoff value for event-free survival in patients with non-ischemic cardiomyopathy (NICM) who had severely reduced LVEF. Materials and Methods: Our prospective cohort study included 78 NICM patients with significantly reduced LV systolic function (LVEF < 35%). CMR images were analyzed for the presence and extent of late gadolinium enhancement (LGE). The primary outcome was major adverse cardiac events (MACEs), defined as a composite of cardiac death, heart transplantation, implantable cardioverter-defibrillator discharge for major arrhythmia, and hospitalization for congestive heart failure within 5 years after enrollment. Results: A total of 80.8% (n = 63) of enrolled patients had LGE, with the median LVEF of 25.4% (19.8-32.4%). The extent of myocardial scarring was significantly higher in patients who experienced MACE than in those without any cardiac events (22.0 [5.5-46.1] %LV vs. 6.7 [0-17.1] %LV, respectively, p = 0.008). During follow-up, 51.4% of patients with LGE ≥ 12.0 %LV experienced MACE, along with 20.9% of those with LGE ≤ 12.0 %LV (log-rank p = 0.001). According to multivariate analysis, LGE extent more than 12.0 %LV was independently associated with MACE (adjusted hazard ratio, 6.71; 95% confidence interval, 2.54-17.74; p < 0.001). Conclusion: In NICM patients with significantly reduced LV systolic function, the extent of LGE is a strong predictor for long-term adverse cardiac outcomes. Event-free survival was well discriminated with an LGE cutoff value of 12.0 %LV in these patients.

• Biomolecules & Therapeutics
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• v.18 no.2
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• pp.135-144
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• 2010

The pro-oxidative and pro-inflammatory pathways in vascular endothelium have been implicated in the initiation and progression of atherosclerosis. In fact, inflammatory responses in vascular endothelium are primarily regulated through oxidative stress-mediated signaling pathways leading to overexpression of pro-inflammatory mediators. Enhanced expression of cytokines, chemokines and adhesion molecules in endothelial cells and their close interactions facilitate recruiting and adhering blood leukocytes to vessel wall, and subsequently stimulate transendothelial migration, which are thought to be critical early pathologic events in atherogenesis. Although interleukin-4 (IL-4) was traditionally considered as an anti-inflammatory cytokine, recent in vitro and in vivo studies have provided robust evidence that IL-4 exerts pro-inflammatory effects on vascular endothelium and may play a critical role in the development of atherosclerosis. The cellular and molecular mechanisms responsible for IL-4-induced atherosclerosis, however, remain largely unknown. The present review focuses on the distinct sources of IL-4-mediated reactive oxygen species (ROS) generation as well as the pivotal role of ROS in IL-4-induced vascular inflammation. These studies will provide novel insights into a clear delineation of the oxidative mechanisms of IL-4-mediated stimulation of vascular inflammation and subsequent development of atherosclerosis. It will also contribute to novel therapeutic approaches for atherosclerosis specifically targeted against pro-oxidative and pro-inflammatory pathways in vascular endothelium.

• Archives of Plastic Surgery
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• v.43 no.1
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• pp.19-25
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• 2016

Background The vermilion plays an important role in both the aesthetic and functional aspects of facial anatomy. Due to its structural features, the complete excision of vascular anomalies on the vermilion is challenging, making it difficult to determine the appropriate treatment strategy. Thus, the authors analyzed the results of surgical treatment of vascular anomalies on the vermilion. Methods The medical records of 38 patients with vascular anomalies on the vermilion who underwent surgery from 1995 to 2013 were analyzed. Nine of the cases had an involuted hemangioma, and 29 cases had a vascular malformation; of the vascular malformations, 13, 11, one, and four cases involved were capillary malformations (CMs), venous malformations (VMs), lymphatic malformations (LMs), and arteriovenous malformations (AVMs), respectively. We investigated the surgical methods used to treat these patients, the quantity of surgical procedures, complications and instances of recurrence, and self-assessed satisfaction scores. Results A total of 50 operations were carried out: 28 horizontal partial excisions, eight vertical partial excisions, and 14 operations using other surgical methods. All cases of AVM underwent complete excision. Six cases experienced minor complications and one case of recurrence was observed. The overall average satisfaction score was 4.1 out of 5, while the satisfaction scores associated with each lesion type were 4.2 for hemangiomas, 3.9 for CMs, 4.2 for VMs, 5.0 for LMs, and 4.0 for AVMs. Conclusions It is difficult to completely excise vascular anomalies that involve the vermilion. This study suggests that partial excision focused on correcting the overall contour of the lips is effective and leads to satisfactory results.

• Archives of Reconstructive Microsurgery
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• v.2 no.1
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• pp.13-19
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• 1993

Although the etiology of $Kienb\"{o}ck's$ disease is clearly related to avascular changes in the lunate, but the actual cause leading to this vascular impairment has remained elusive. Therefore, a great many different surgical procedures have been proposed for the correction of the multiple factors leading to lunate collapse or for the treatment of the lunatomalacia. The treatment modalities includes lunate excision, intercarpal arthrodesis, lunate implant resection arthroplasty, joint levelling operation(e.g ulnar lengthening & radial shortening), pronater quadratus pedicle graft and vascular loop graft. In the period from Jan. 1981 to Dec. 1992, we performed operative treatment in 19 cases of $Kienb\"{o}ck's$ disease. Among them, 6 cases were treated with vascular loop graft. We analysed all patients who were treated with vascular loop graft after followed up of 4 year 6 months, on an average(range from 1 year to 8 year 10 months). The results analysed are as follows, 1. All cases were stage III according to Lichtman's classification. 2. Ulnar variance was -1.5(range$-2{\sim}0$), on an average. 3. The average age of patients were 37.7years old(range 31-41). 4. Postoperatively, there were considerable restoration of range of motion and complete relief of pain in all cases, but continued decrease of grip power in one case. 5. Decreased sclerosis, loss of fragmentation and new bone formation were appeared in the last follow up film, in all cases. The vascular loop graft considered as a useful method for the treatment of the $Kienb\"{o}ck's$ disease.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.6
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• pp.641-647
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• 2016

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.1
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• pp.63-68
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• 2013

Background: Tumor angiogenesis correlates with recurrence and appears to be a prognostic factor for both breast and prostate cancers. In the present study, we aimed to investigate the correlation of microvessel density (MVD), a measure of angiogenesis, with nuclear pleomorphism, mitotic count, and vascular invasion in breast and prostate cancers at preclinical and clinical levels. Methods: Samples from xenograft tumors of luminal B breast cancer and prostate adenocarcinoma, established by BT-474 and PC-3 cell lines, respectively, and commensurate human paraffin-embedded blocks were obtained. To determine MVD, specimens were immunostained for CD-34. Nuclear pleomorphism, mitotic count, and vascular invasion were determined using hematoxylin and eosin (H&E)-stained slides. Results: MVD showed significant correlations with nuclear pleomorphism (r=0.68, P=0.03) and vascular invasion (r=0.77, P=0.009) in breast cancer. In prostate cancer, MVD was significantly correlated with nuclear pleomorphism (r=0.75, P=0.013) and mitotic count (r=0.75, P=0.012). In the breast cancer xenograft model, a significant correlation was observed between MVD and vascular invasion (r=0.87, P=0.011). In the prostate cancer xenograft model, MVD was significantly correlated with all three parameters (nuclear pleomorphism, r=0.95, P=0.001; mitotic count, r=0.91, P=0.001; and vascular invasion, r=0.79, P=0.017; respectively). Conclusions: Our results demonstrate that MVD is correlated with nuclear pleomorphism, mitotic count, and vascular invasion at both preclinical and clinical levels. This study therefore supports the predictive value of MVD in breast and prostate cancers.

• The Journal of Internal Korean Medicine
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• v.19 no.2
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• pp.50-59
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• 1998

Background : Vascular dementia occurs mainly due to cerebral vascular disease. So we performed this clinical study to investigate the incidence and characteristics of vascular dementia in stroke patients. Methods : This study was performed on the patients hospitalized from April 1, 1998 to August 31, 1998 at the department of circulatory internal medicine, hospital of Oriental medicine, Kyung-Hee University, and diagnosed cerebral infarction or hemorrhage by Brain CT or MRI. we devided the patients into two groups; vascular dementia group and non dementia group according to MMSE-K(Mini Mental State Examination Korean version), Hasegawa dementia scale. Patients were diagnosed dementia using DSM-IV. We compared general characteristics, stoke types and laboratory findings between the two groups and investigated the correlationship between MMSE-K and Hasegawa dementia scale. Results : Results showed that the incidence of vascular dementia was about 27.8% in stroke patients. The greater number of subjects with dementia were women in the lower educational classes and had lower MBI(Moderfied Bathel Index) scores. Vascular dementia were more common in patients with large brain lesion size($>20cm^3$). There was a positive correlationship between Hasegawa scores and MMSE-K.

• Molecules and Cells
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• v.41 no.3
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• pp.198-206
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• 2018

Aortic dissection (AD) is a catastrophic disease with high mortality and morbidity, characterized with fragmentation of elastin and loss of smooth muscle cells. Although AD has been largely attributable to polymorphisms defect in the elastin-coding gene, tropoelastin (TE), other undermined factors also appear to play roles in AD onset. Here, we investigated the effects of post-transcriptional control of TE by microRNAs (miRNAs) on elastin levels in aortic smooth muscle cells (ASMC). We found that miR-144-3p is a miRNA that targets TE mRNA in both human and mouse. Bioinformatics analyses and dual luciferase reporter assay showed that miR-144-3p inhibited protein translation of TE, through binding to the 3'-UTR of the TE mRNA. Interestingly, higher miR-144-3p levels and lower TE were detected in the ASMC obtained from AD patients, compared to those from non-AD controls. In a mouse model for human AD, infusion of adeno-associated viruses (serotype 6) carrying antisense for miR-144-3p (asmiR-144-3p) under CAG promoter significantly reduced the incidence and severity of AD, seemingly through enhancement of TE levels in ASMC. Thus, our data suggest an essential role of miR-144-3p on the pathogenesis of AD.