No abstract available.
Emphysema* ; Tuberculosis*

BACKGROUND: Because systolic and diastolic dysfunction frequently coexist in acute myocardial infarction(AMI), we hypothesize that a combined measure of ventricular performance using Doppler echocardiography may be more sensitive and time-saving diagnostic tool for the evaluation of patients presenting with cardiogenic chest pain. METHOD AND RESULTS: Seventy-one patients with AMI (47 male, 59+/-11 years) and 45 patients with normal coronary artery (29 male, 52+/-11 years) were included in the study for measurement of cardiac performance index and established parameters of ventricular function using conventional echo-Doppler methods. a new derived index of cardiac performance: (ICT+IRT)/ET, was obtained by subtracting ejection time(ET) from the interval between cessation and onset of the mitral inflow velocity to give the sum of isovolumic contraction time(ICT) and isovolumic relaxation time(IRT). The mean value of the index was significantly different between normal and AMI(p<0.01). The degree of inter-group overlap was smaller for the index compared to other parameters. within functional groups, the value of the index did not appear to be related to heart rate, mean arterial pressure and the degree of mitral regurgitation. CONCLUSION: cardiac performance index is a conceptually new, simple and reproducible Doppler index of combined systolic and diastolic myocardial performance, and it is useful as screening test for patients with cardiac dysfunction due to AMI.
Arterial Pressure ; Chest Pain ; Coronary Vessels ; Echocardiography, Doppler ; Heart Rate ; Humans ; Male ; Mass Screening* ; Mitral Valve Insufficiency ; Myocardial Infarction* ; Relaxation ; Ventricular Function

Acetabular bone deficiencies encountered during the revision hip arthroplasties should be recon- structed to provide the implant stability and to restore the normal center of rotation of hip and the leg length. We revised the loosened acetabular cup by grafting fresh-frozen bulk femoral head and inserting uncemented cup in 17 hips of 15 patients. The average follow-up period was 2 years and 3 months. The acetabular bone deficiencies were type 2A in 6 hips, type 2B in 8, type 3A in 1 and type 3B in 2 by Paprosky's classification. Three blocks of femoral head were grafted in 3 type 3 deficiencies, but only one in type 2 deficiencies. The cup-host bone contact was 41% on the average. However, the cup-host bone contact in the zone I was present only in 12 out of 17 hips and its average was 14%. Incorporation of the allograft into the host bone occurred between 5 months and 1 year and 7 months (average, 8,6 months) after revision surgery. Significant radiographic loosening sign was noted only in 2 hips which had not only type 3B bone deficiencies reconstructed with 3 blocks of femoral head allograft but also no cup-host bone contact in zone I . The bulk allograft of fresh-frozen femoral head demonstrated acceptable results in type 2 acetabular bone deficiencies, although the follow-up period was relatively short. Reconstruction of type 3B acetabular bone deficiencies by using multiple blocks of femoral head allograft had been failed. We presumed that the lack of the graft stability and the intimate contact between the grafts and host bone was the cause of failure.
Acetabulum* ; Allografts* ; Arthroplasty ; Classification ; Follow-Up Studies ; Head* ; Hip ; Humans ; Leg ; Transplants

Since nonsurgical treatment of vitiligo is not always successful, surgical interventions are viable options for patients with refractory vitiligo. Surgical treatment is a method in which melanocytes of normal skin are transplanted into vitiligo lesions and provided as a repigmentation source. Such treatments are primarily divided into tissue grafting and cellular grafting, depending on the nature of the graft. Tissue grafting includes split-thickness skin grafting, suction blister grafting, punch grafting, hair follicle transplantation, and smashed-skin grafting. Cellular grafting includes non-cultured epidermal cell suspension transplantation, non-cultured follicular cell suspension transplantation, and cultured epidermal cell suspension transplantation. Among these, suction blister grafting and micro-punch grafting have been widely performed for localized refractory vitiligo, and non-cultured epidermal cell suspension transplantation is adopted as the standard treatment for extensive vitiligo. Research on cultured cellular grafting to treat larger vitiligo areas is also ongoing. Selecting patients with stable vitiligo that has not spread for over 12 months is the most critical factor in the surgical outcome. It is also important to choose an appropriate surgical modality for each patient, and a combination of various procedures often improves the overall outcome. In conclusion, surgical intervention can be an effective and safe option for patients with vitiligo refractory to conventional treatments. Non-cultured epidermal cell suspension transplantation, which was denied by New Health Technology Assessment in Korea, should be approved to benefit patients with refractory vitiligo.

Since nonsurgical treatment of vitiligo is not always successful, surgical interventions are viable options for patients with refractory vitiligo. Surgical treatment is a method in which melanocytes of normal skin are transplanted into vitiligo lesions and provided as a repigmentation source. Such treatments are primarily divided into tissue grafting and cellular grafting, depending on the nature of the graft. Tissue grafting includes split-thickness skin grafting, suction blister grafting, punch grafting, hair follicle transplantation, and smashed-skin grafting. Cellular grafting includes non-cultured epidermal cell suspension transplantation, non-cultured follicular cell suspension transplantation, and cultured epidermal cell suspension transplantation. Among these, suction blister grafting and micro-punch grafting have been widely performed for localized refractory vitiligo, and non-cultured epidermal cell suspension transplantation is adopted as the standard treatment for extensive vitiligo. Research on cultured cellular grafting to treat larger vitiligo areas is also ongoing. Selecting patients with stable vitiligo that has not spread for over 12 months is the most critical factor in the surgical outcome. It is also important to choose an appropriate surgical modality for each patient, and a combination of various procedures often improves the overall outcome. In conclusion, surgical intervention can be an effective and safe option for patients with vitiligo refractory to conventional treatments. Non-cultured epidermal cell suspension transplantation, which was denied by New Health Technology Assessment in Korea, should be approved to benefit patients with refractory vitiligo.

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*

BACKGROUND: To investigate the role of alpha-adrenergic receptors in the development of delayed afterdepolarization, the effect of alpha-adrenoceptor stimulation and blockade on ouabain induced delayed afterdepolarization(DDAD) was examined in rabbit heart Purkinje fibers. METHODS: Purkinje fibers, taken from adult rabbit(1.8 - 2.0kg) heart anesthetized with penobarbital, were mounted in a Luicite chamber and superfused with Tyrode's solution. The transmembrane potentials were measured by the conventional microelectrode technique while the fibers were being stimulated with rectangular pulses of 50% above threshold voltage. The delayed afterdepolarizations were induced by overdrive excitation in the presence of ouabain. RESULTS: Delayed afterdepolarizations were not observed during superfusion of the control Tyrode's solution containing propranolol(5x10(-7)M). However, the addition of ouabain in the presence of propranolol elicited DADs which were dose-, time- and drive cycle length- dependent. Phenylephrine(PE ; 10(-7)M), and alpha-adrenoceptor agonist, potentiated the ouabain-induced DAD during the initial superfusion(for 10 or 20 min) of the test Tyrode's solution. However, it was followed by attenuating-effects after a superfusion time of 50 to 60 min. Both effects showed ouabain dose-dependence. Ouabain(2x10(-7)M), in the presence of propranolol, depolarized the maximum diastolic potential and shortened the action potential duration, and the addition of PE(10(-7)M) did not affect the characteristics of action potential except a decrease in velocity of phase 0 depolarization. Prazosin, an alpha1-adrenoceptor antagonist, inhibited the PE's enhancing effects of ouabaininduced DDAD at 20 min superfusion, but did not affect the attenuating-effects of PE at 60 min superfusion. On the other hand, yohimbine, an alpha2-adrenoceptor antagonist, did not affect the PE's DAD potentiating-effects at 20 min superfusion, but inhibited the attenunating-effects of PE at 60 min superfusion. CONCLUSION: It is inferred that alpha-adrenergic stimulation induce delayed afterdepolarization and triggered activity in the rabbits, being responsible for the arrhythmia development, and the effects are mainly due to the action of alpha1-subtpe adrenoceptor stimulation.
Action Potentials ; Adult ; Arrhythmias, Cardiac ; Hand ; Heart ; Humans ; Membrane Potentials ; Microelectrodes ; Ouabain ; Prazosin ; Propranolol ; Purkinje Fibers ; Rabbits ; Receptors, Adrenergic, alpha* ; Yohimbine

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.
Acetylcholine ; Action Potentials ; Adenosine ; Animals ; Atropine ; Carbachol ; Cholinergic Agonists* ; Hand ; Ischemia ; Microelectrodes ; Myocardium* ; Rats*

PURPOSE: Kabuki syndrome is a multiple congenital malformation syndrome with mental retardation. It was named after its characteristic appearance, a face resembling that of an actor in a Kabuki play. To date, six Korean cases of Kabuki syndrome have ever been reported. Here, we present the phenotypic and genetic characteristics of six patients with Kabuki syndrome. MATERIALS AND METHODS: Between 2003 and 2009, six Korean girls have been diagnosed and followed up as Kabuki syndrome at Center for Genetic Diseases of Ajou University Hospital. Their clinical and laboratory data were collected and analyzed by the retrospective review of medical records. RESULTS: All six patients showed the characteristic facial dysmorphism and developmental delay. Persistent fingertip pads were also found in all patients. Most patients showed postnatal growth retardation (83.3%) and hypotonia (83.3%). Opthalmologic problems were common, particularly for strabismus (83.3%). Congenital heart defects were present in three patients (50%). Skeletal abnormalities including 5th finger shortening (83.3%), clinodactyly (50%), joint hypermobility (50%) and hip dislocation (16.7%) were also observed. There was no patient who had positive family history for Kabuki syndrome. Cytogenetic and molecular cytogenetic analyses including karyotyping and array CGH could not reveal any underlying genetic cause of Kabuki syndrome. CONCLUSION: Korean patients with Kabuki syndrome showed a broad spectrum of clinical features affecting multiple organ systems. Although clinical manifestations of Kabuki syndrome have been well established, our results failed to detect recurrent chromosome aberrations which could cause Kabuki syndrome. Its natural history and genetic background remains to be further studied for providing appropriate management and genetic counseling.
Abnormalities, Multiple ; Child ; Chromosome Aberrations ; Cytogenetic Analysis ; Cytogenetics ; Face ; Fingers ; Genetic Counseling ; Heart Defects, Congenital ; Hematologic Diseases ; Hip Dislocation ; Humans ; Intellectual Disability ; Joint Instability ; Karyotyping ; Medical Records ; Muscle Hypotonia ; Natural History ; Retrospective Studies ; Strabismus ; Vestibular Diseases

Background: and Purpose This study aimed to determine the effects of oxcarbazepine (OXC) on the language function of patients with pediatric epilepsy. Methods: We assessed the language abilities of patients aged 5–17 years with newly diagnosed focal epilepsy and the same number of age-matched healthy children using the Test of Problem Solving (TOPS) and the Receptive and Expressive Vocabulary Test–Receptive (REVT-R). The Mean Length of Utterance–words (MLU-w) was used to estimate linguistic productivity before and after OXC initiation. All patients received OXC monotherapy with a starting dosage of 10 mg/kg/day for 1 week, which in some cases was increased to 30 mg/kg/ day (or 1,200 mg/day). Results: The study finally included 41 pediatric patients (22 males and 19 females; age 9.9±3.0 years, mean±standard deviation). All language parameters of the TOPS improved significantly after initiating OXC (determining cause, 12.5±4.8–13.7±4.1 [p=0.016]; making inference, 15.6±5.6–17.4±6.4 [p<0.001]; and predicting, 9.8±5.0–11.6±4.5 [p=0.001]). However, patients who received OXC did not exhibit a significantly extended MLU-w (determining cause, p=0.493; making inference, p=0.386; and predicting, p=0.341). Receptive language scores also significantly increased after taking OXC (REVT-R: 121.0±43.1–129.4±43.8, p=0.002), but the percentage of development age to chronological age did not vary (REVT-developmental quotient: p=0.075). Conclusions Our results suggest that OXC is safe and preserves language function in patients with pediatric epilepsy.