Objective: : This study aimed to assess the relationship between increased intracranial pressure (ICP) and mastoid effusions (ME). Methods: : Between January 2015 and October 2018, patients who underwent intracranial surgery and had ICP monitoring catheters placed were enrolled. ICP was recorded hourly for at least 3 days. ME was determined by the emergence of opacification in mastoid air cells on follow-up brain imaging. C-reactive protein (CRP) levels, presence of endotracheal tube (ETT) and nasogastric tube (NGT), duration of intensive care unit (ICU) stay, duration of mechanical ventilator application, diagnosis, surgical modalities, and presence of sinusitis were recorded. Each factor’s effect on the occurrence of ME was analyzed by binary logistic regression analyses. To analyze the independent effects of ICP as a predictor of ME a multivariable logistic regression analysis was performed. Results: : Total of 61 (53%) out of 115 patients had ME. Among the patients who had unilateral brain lesions, 94% of subject (43/50) revealed the ipsilateral development of ME. ME developed at a mean of 11.1±6.2 days. The variables including mean ICP, peak ICP, age, trauma, CRP, ICU stays, application of mechanical ventilators and presence of ETT and NGT showed statistically significant difference between ME groups and non-ME groups in univariate analysis. Sex and the occurrence of sinusitis did not differ between two groups. Adding the ICP variables significantly improved the prediction of ME in multivariable logistic regression analysis. Conclusion : While multiple factors affect ME, this study demonstrates that ICP and ME are probably related. Further studies are needed to determine the mechanistic relationship between ICP and middle ear pressure.

BACKGROUND AND OBJECTIVES: Regression of left ventricular hypertrophy (LVH) is important because development of myocardial ischemia, heart failure or arrhythmias may be reduced. However, an animal model for LVH regression is not well established and there are no useful parameters to predict LVH regression. Magnetocardiogram (MCG), magnetic signal generated from the heart, has recently been investigated for the detection of electrical current changes of the heart. This study was undertaken to establish rat models of LVH-regression and to assess MCG changes during LVH induction and regression. MATERIALS AND METHODS: Rat models of pressure overload LVH were established by transverse aortic constriction (TAC) and LVH regression was generated by untying 2 weeks after TAC. Hemodynamic, echocardiographic and biochemical evaluation were performed in order to confirm this model. Magnetic fields were recorded with a SQUID gradiometer before and after TAC, and also recorded at 1, 3, 7, and 14 days after untying, respectively. RESULTS: Rat models of LVH-regression were established successfully by TAC and untying. The pressure gradient across TAC disappeared within 10 minutes after untying. LV weight, LV weight/body weight ratio, LV mass and expression level of atrial natriuretic factor were significantly increased following TAC and decreased to baseline value after pressure unloading. Deeper S waves and strain patterns were observed after LVH induction and gradually returned to basal levels over the 2 weeks after untying. CONCLUSION: MCG changes in the rat models of LVH-regression indicate that MCG can be a helpful modality for the diagnosis and evaluation of LVH as well as follow-up after treatment of LVH.
Animals ; Arrhythmias, Cardiac ; Atrial Natriuretic Factor ; Constriction ; Decapodiformes ; Diagnosis ; Echocardiography ; Follow-Up Studies ; Heart ; Heart Failure ; Hemodynamics ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Magnetic Fields ; Models, Animal ; Myocardial Ischemia ; Rats*

BACKGROUND AND OBJECTIVES: Although it is well known that mitral valve repair provides a better postoperative outcome than valve replacement for mitral valve prolapse with mitral regurgitation, there haven't been much studied the nature of remnant regurgitation and the change of heart function and structure by remnant regurgitation after mitral valve repair surgery. We tried to research for it. METHODS AND RESULTS: Retrospective analysis of echocardiographic data and medical records was done in patients who underwent repair surgery for mitral valve prolapse with significant mitral regurgitation at the Keimyung University Dong-san Medical Center from February 1996 to February 2000. Patients who underwent echocardiography before and after the surgery were selected for the analysis. Of patients who underwent mitral valve repair surgery for mitral valve prolapse with mitral regurgitation during that period, 30 patients (male 15, female 15) were included in this study. The average age of them was 44.30+/-14.30 year old. After surgery, heart chamber size was decreased significantly in all patients (e. g. LVDd 6.25+/-1.06 cm vs. 5.14+/-0.62 cm, LV mass 272.46+/-107.36 gm vs. 197.30+/-75.16 gm). Remnant mitral regurgitation after repair surgery was found in 22 patients (73.3%). Remnant mitral regurgitation above trivial flow was found in 10 patients. Such case as involving ant. leaflet was found in 5 patients (16.7%), as involving post. leaflet, in 2 patients (6.7%), as involving both leaflet, in 3 patients (10%) among 10 ones. Eccentric flow among remnant regurgitation, was observed in 2 patients who underwent repair surgery for ant. leaflet, 1 patient who underwent repair surgery for both leaflet. CONCLUSION: Mitral valve repair surgery reduce the left ventricular chamber size and left ventricular mass. Postoperatively, patients who involve ant. leaflet were much remnant regurgitation above trivial flow more than others.
Ants ; Echocardiography ; Female ; Heart ; Humans ; Medical Records ; Mitral Valve Insufficiency* ; Mitral Valve Prolapse* ; Mitral Valve* ; Retrospective Studies ; Thoracic Surgery

BACKGROUND AND OBJECTIVES: Ischemic injury is the most common and important cause of myocardial damage. Over past decades, a number of studies have identified a protective mechanism known as ischemic preconditioning, which can block or delay cell death from ischemic injury. Protein kinase C (PKC), especially theepsilonisoform has been proposed as a key factor in the signaling pathway of ischemic preconditioning. However, whether PKCepsilon expression in cardiomyocytes can offer such protection from acute ischemia has not been explored. MATERIALS AND METHODS: To demonstrate a direct effect of PKCepsilon expression, a lentiviral vector system was established. Using the lentiviral vector, PKCepsilon was introduced to neonatal rat ventricular myocytes (NRVM) cultured under ischemic conditions, and also to adult rat myocardium subject to left coronary artery ligation. RESULTS: Compared to control, PKCepsilon expression in cultured NRVM under ischemia resulted in preserved cell density and morphology, and a reduction in cell death (77.6+/-12.8% vs 58.1+/-7.2%, p<0.05). In adult rats, the infarcted area after coronary artery ligation was markedly reduced in myocardium injected with PKCepsilon vector compared to control (11.4+/-5.3% vs 20.5+/-11.3%, p<0.01). CONCLUSION: These results provide direct evidence that PKCepsilon is a central player in protection against cell death from acute ischemia.
Adult ; Animals ; Cell Count ; Cell Death ; Coronary Vessels ; Humans ; Ischemia ; Ischemic Preconditioning ; Lentivirus ; Ligation ; Muscle Cells ; Myocardium ; Myocytes, Cardiac* ; Protein Kinase C ; Protein Kinase C-epsilon ; Protein Kinases* ; Rats

BACKGROUND AND OBJECTIVES: Rapamycin has been shown to inhibit the vascular smooth muscle cell migration and proliferation that contributes to neointimal formation. We investigated whether the perivascular delivery of rapamycin in Pluronic gel could inhibit neointimal hyperplasia in a rat carotid artery model, and we tested the usefulness of carotid arteriography. MATERIALS AND METHODS: To assess the kinetics of rapamycin's release from Pluronic gel, a [3H] thymidine incorporation assay was performed with using the media exposed to rapamycin in Pluronic gel for 10, 20, 60 and 120 min. We applied 100 microgram of rapamycin in Pluronic gel to the perivascular space of the carotid artery after the balloon injury (n=9), whereas only gel was applied in a control group (n=9). We performed the carotid arteriography and the morphometric analysis 14 days after injury. RESULTS: The [3H] thymidine incorporation assay showed a reduction of uptake in a time-dependent manner (86%, 48%, 45% and 40% of the control, respectively, at 10, 20, 60 and 120 minutes). The inhibiting effect of rapamycin on neointimal hyperplasia was identified on the carotid arteriography (mean luminal diameter; 0.75+/-0.11 vs. 0.60+/-0.12 arbitrary units, respectively, p< 0.05) and on the morphometric analysis (neointima area: 0.09+/-0.03 vs. 0.17+/-0.06 mm(2), respectively, p< 0.05). CONCLUSION: This study demonstrated that perivascular delivery of rapamycin in Pluronic gel inhibits neointimal hyperplasia in a rat carotid injury model. This animal model combined with arteriography can be used for developing new drugs to treat restenosis. In addition, this technique might be useful for vascular surgery such as coronary artery bypass grafting, arteriovenous fistula formation and peripheral vascular bypass graft insertion.
Angiography ; Animals ; Arteriovenous Fistula ; Carotid Arteries ; Carotid Artery Injuries ; Cell Movement ; Coronary Artery Bypass ; Drug Delivery Systems ; Hyperplasia ; Kinetics ; Models, Animal ; Muscle, Smooth, Vascular ; Phenobarbital ; Rats ; Sirolimus ; Thymidine ; Transplants

BACKGROUND AND OBJECTIVES: The degree of neointima formation after infliction of a carotid artery balloon injury in rats varies greatly depending on the sex, age, species and operational method. Strong variation is common, even within only a single control. This study attempted to find if there was any significant difference in neointima formation following a carotid artery balloon injury in 6 to 12 week old rats; the age commonly used in these types of experiments. MATERIALS AND METHODS: A balloon injury was inflicted on the carotid arteries of male SpragueDawley rats at 6 (n=9, 250-270 g), 8 (n=8, 280-300 g) and 11 weeks (n=10, 320-340 g) of age. Two weeks postoperation, a histomorphometric analysis was carried out. The vascular smooth muscle cell proliferation was measured in situ via BrdU incorporation 2 days after injury infliction. RESULTS: The neointima areas of the 6 week (0.22+/-0.04 mm2) and 8 week old groups (0.17+/-0.08 mm2) were 3.1 and 2.4 times larger than that of the 11 week old group (0.07+/-0.03 mm2). The mitotic index was significantly reduced in 11 week old group (n=4, 9.22+/-1.51%) compared to those of the 6 (n=4, 25.03+/-3.92%) and 8 week old (n=4, 21.66+/-3.66%) groups. CONCLUSION: Special care should be taken when interpreting neointima formation, as even a slight variation in the age and weight in 6 to 12 week old (250-340 g) rats; the age commonly used in these types of experiments, results in an unexpectedly large difference.
Aging ; Animals ; Bromodeoxyuridine ; Carotid Arteries* ; Carotid Artery Injuries* ; Cell Proliferation ; Humans ; Male ; Mitotic Index ; Muscle, Smooth, Vascular ; Neointima* ; Rats*

Primary biliary cirrhosis (PBC) is a chronic progressive disease, more often affecting women, characterised by progressive destruction of the small intrahepatic bile ducts with portal inflammation leading to fibrosis and cirrhosis. There is a close association between PBC and antibodies to antimitochondrial antibodies (AMA). The pathogenesis of PBC remains uncertain. The disease has been considered as an example of autoimmunity. Estimates of disease prevalence vary between 20 and 240 cases per milion per year. PBC is a extremely rare liver disease in Asia. There is no definitive drug treatment, liver transplantation is indicated for patients with intractable symptoms and for end-stage disease. The authors have experienced a case of PBC in 66 year-old female who suffered from lethargy, pruritus and dry mouth since 2 years ago. We report a case of PBC with a review of literatures.
Aged ; Antibodies ; Asia ; Autoimmunity ; Bile Ducts, Intrahepatic ; Female ; Fibrosis ; Humans ; Inflammation ; Lethargy ; Liver Cirrhosis, Biliary* ; Liver Diseases ; Liver Transplantation ; Mouth ; Prevalence ; Pruritus

BACKGROUND AND OBJECTIVES: The Vascular system exhibits altered morphological and functional properties during hypertension and after anti-hypertensive therapy. To characterize such changes, the contractile, histological and molecular responses in the common carotid arteries (CCA) were compared in 35 rats. MATERIALS AND METHODS: By partial transverse aortic constriction (TAC), the right CCAs were made to lie under a high pressure environment, while the left CCAs remained under normotension, the latter being used as control vessels. The ligations were removed after two weeks, to enable the recovery process to begin. RESULTS: The vessel contractility, two weeks after the TAC, was nearly abolished. The recovery process from high pressure showed an initial hypercontractile period of around 1-2 week after recovery, prior to the subsequent decline to a normal contractility after 2 weeks. The relaxation response due to acetylcholine was minimal at the end of the hypertensive period, recovered slowly, and reached a normal magnitude after 4 weeks. A high pressure increases the medial thickness & area, and enhances the adventitial tissue formation. These changes persist during the first 4 weeks of recovery, after which normotension returns. Apoptosis at the endothelial layer was significantly increased two weeks after the TAC, but normalized two weeks after recovery. The expression of ecNOS was not detect 2 weeks after the TAC, but gradually returned to a basal level at 2 weeks after the untying. CONCLUSION: A high blood pressure causes decreases in the contractility and endothelium-dependent relaxation. It also increases endothelial apoptosis, the medial thickness & area, and enhances the adventitial tissue formation. The recovery processes from high blood pressure are not uniform, but show different normalizations among the structural, contractile and apoptotic parameters.
Acetylcholine ; Adventitia ; Animals ; Apoptosis ; Arteries ; Carotid Arteries* ; Carotid Artery, Common ; Constriction ; Hypertension ; Ligation ; Nitric Oxide ; Rats* ; Relaxation

BACKGROUND AND OBJECTIVES: The roles of angiotensin II (Ang II) in the regulation of heart function under normal and pathological conditions have been well documented, with its biological actions mainly mediated via the Ang II type 1A receptor (AT(1A)R). Since the inhibition of the renin-angiotensin system can prevent or regress left ventricular hypertrophy (LVH) with hypertension, AT(1A)R-mediated signaling is considered one of the important transcriptional pathways in the development of cardiac hypertrophy. SUBJECTS AND METHODS: To address whether AT(1A)R-mediated signaling plays an important role in the development of pressure overload-induced LVH and fibrosis, the physiological, biochemical, hemodynamic and histopathological parameters were evaluated before and after transverse aortic constriction (TAC) in wild-type (WT) and AT(1A)R knockout (KO) mice. RESULTS: Although the LV systolic pressure (83.2+/-10.0 mmHg, n=5) of the KO mice was lower than that (90.0+/-5.0 mmHg, n=7) of the WT mice, there was no difference in the increase in the LV systolic pressure between the WT and KO mice (WT, 42.0 mmHg; KO, 41.8 mmHg). Also, there was no difference between the baseline LV-to-body weight (LVW/BW) ratio between the two groups (WT, 3.10+/-0.21 mg/g; KO 3.04+/-0.21 mg/g). Two weeks after TAC, the degree of increase in the LVW/BW ratio was markedly increased in both the WT (4.17+/-0.28 mg/g, n=9) and KO mice (4.16+/-0.43 mg/g, n=8), which were almost identical (WT, 34.5%; KO, 36.8%). There were no significant differences in the LV end-diastolic pressure, LV+dP/dt(max), and heart rate between the two groups. The ERK44/42 and p38-MAPK activities in the LV were markedly increased by TAC in both groups, but that of JNK was not. Interstitial and perivascular fibrosis developed in both groups following TAC. However, the degree of increased fibrosis was significantly attenuated in the KO mice. CONCLUSION: These results suggest AT(1A)R-mediated signaling is not indispensable for the development of pressure overload-induced LVH, and provides new insights into the development of novel therapeutic strategies for cardiac hypertrophy.
Angiotensin II* ; Angiotensins* ; Animals ; Blood Pressure ; Cardiomegaly ; Constriction ; Fibrosis* ; Heart ; Heart Rate ; Hemodynamics ; Hypertension ; Hypertrophy, Left Ventricular* ; Mice ; Renin-Angiotensin System

The purpose of our study was to create a novel rat aorta stent implantation model. Stainless steel bare metal stents (BMS) or paclitaxel-eluting stents (PES) were implanted in male Sprague-Dawley rats (BW 400 +/- 20 g). Two and four weeks after stent implantation, the aorta were collected, fixed with 2% glutaraldehyde, and cut into two segments. One segment was used for scanning electron microscopy analysis to evaluate re-endothelialization, and the other segment was used to calculate the neointimal area. At 2 weeks after stenting, the appearance of neointimal hyperplasia was less in the PES group than in the BMS group. At 4 weeks after stenting, no significant difference in neointimal hyperplasia was observed between two groups. On the other hand, the PES group showed more thrombus formation and less re-endothelialization compared to the BMS group. This study demonstrated the ability of a novel rat model of aorta stenting via a common carotid artery to measure the efficacy and safety of commercially available drug-eluting stents.
Angioplasty/*methods ; Animals ; Aorta, Thoracic/*surgery/ultrastructure ; Coronary Artery Disease/*surgery ; *Drug-Eluting Stents ; Histocytochemistry ; Male ; Microscopy, Electron, Scanning ; Models, Animal ; Neointima/pathology ; Paclitaxel/*administration & dosage ; Rats ; Rats, Sprague-Dawley