No abstract available.
Animals* ; Leptospirosis*

No abstract available.
Animals* ; Leptospirosis*

C-fos protein is a gene regulatory third messenger involved in long-term responses of cells to various stimuli. Kainic acid(KA), a powerful excitatory analogue, induces seizures and damages the hippocampus and other limbic regions in rats. KA treatment induces c-fos protein production in the hippocampus. This study was undertaken to investigate the expression of c-fos protein in the hippocampus according to seizure stage induced by systemic injection of KA. Twenty-three adult male Sprague-Dawley rats experienced convulsions by a single intraperitoneal injection of convulsive dose (20-40 mg/Kg) of KA. Seven control rats received normal saline. Animals were sacrificed 3 hr after KA treatment. The expression of c-fos protein was tested in the hippocampus by immunohistochemical staining using polyclonal anti-Fos. Most of the rats exhibited limbic motor epileptic activity. C-fos protein immunoreactivity increased in the CA1, CA3 and dentate gyrus at stage 1-2, and not only in the CA1, CA3 and dentate gyrus but also in the CA4 at stage 3-4. At stage 5, c-fos protein immunoreactivity increased in all areas of the hippocampus. C-fos protein immunoreactivity increased progressively with increasing severity of convulsions. These results show that KA produces limbic motor seizure associated with a rise in the c-fos protein in the hippocampus, and that the expression of c-fos protein may has some relevance to the progressive and permanent brain changes occurring during epilepsy.
Adult ; Animals ; Brain ; Dentate Gyrus ; Epilepsy ; Genes, vif ; Hippocampus* ; Humans ; Injections, Intraperitoneal ; Male ; Rats* ; Rats, Sprague-Dawley ; Seizures*

No abstract available.

OBJECTIVES: To evaluate the cross-sectional area (CSA) and the moment arm length (MAL) of the paraspinal muscles in the degenerative lumbar spondylolisthesis patients compared to the matched control patients, which is through contribution to the stability of the back. MATERIALS AND METHODS: We studied a comprised of 25 degenerative lumbar spondylolisthesis on L4/5 patients and a controlled group with 42 chronic lower back pain patients. In both groups, we measured body mass index (BMI, kg/m2). On the standing lateral radiographs, we measured the total lumbar lordosis, and segmental lumbar lorodosis using Cobb's methods. We measured the degree of slippage by Meyerding classification. The CSA of erector spinae (CSA) and CSA of psoas were measured at the L4/5 level by using the MRI. The statistical analysis were performed to know the relationship between the CSA and the MAL of erector spinae, and the BMI. Multifidus and erector spinae atrophy were evaluated at the L4/5 level and the degree of fatty atrophy was estimated using three grades : mild, moderate, and severe. RESULTS: The patient group and the controlled group BMI (kg/m2) were 25.27+/-3.8 and 24.47+/-3.24. In patient group, Meyerding classification grade I was 92%. Total lumbar lordosis and each segmental lordosis were measured mean angle 44.54degrees(24.9degrees~70.4degrees), and each 9.23degrees(L3/4), 10.27degrees(L4/5), 18.81degrees(L5/S1). Pearson's rho indicated a positive association between the CSA and BMI (rho=0.603, p= 0.001), between the CSA of psoas and BMI (rho=0.445, p=0.026), and between the CSA and MAL (rho=0.627, p=0.001) in the degenerative lumbar spondylolisthesis patients. In terms of the CSA versus MAL, there was a positive association in the both groups (rho=0.627, p=0.001, MAL=0.0008 CSA+/-5.293 in the degenerative lumbar spondylolisthesis group; rho=0.812, p=0.000, MAL=0.001 CSA+/-5.245 in the control group with using linear regression analysis). Independent t-test revealed that both groups had statistically different mean values (p=0.038) in terms of the CSA. Proportion of fat deposits in the multifidus and erector spinae muscle at the L3/4 level were all mild grades. CONCLUSION: The patients with degenerative lumbar spondylolisthesis had atrophied erector spinal muscles, which means harmful because of the poor compensation for the lower back load and poor assists to the lumbar stability. This suggests that the biomechanical factor of the muscles influence to the lumbar disability.
Animals ; Arm ; Atrophy ; Body Mass Index ; Compensation and Redress ; Humans ; Linear Models ; Lordosis ; Low Back Pain ; Muscles ; Spondylolisthesis

Odontogenic infections are a normally locally confined, self-limiting process that is easily treated by antibiotic therapy and local surgical treatment. However, it may spread into the surrounding tissues through a perforation of the bone, and into contiguous fascial spaces or planes like the primary or secondary fascial spaces. If the infection extends widely, it may spread into the lateral pharyngeal and retropharyngeal space. The retropharyngeal space is located posterior to the pharynx. If an odontogenic infection spreads into this space, severe life-threatening complications will occur, such as airway obstruction, mediastinitis, pericarditis, pleurisy, pulmonary abscess, aspiration pneumonia and hematogenous dissemination to the distant organs. The mortality rate of mediastinitis ranges from 35% to 50%. Therefore, a rapid evaluation and treatment are essential for treating retropharyngeal space abscesses and preventing severe complications. Recently, we encountered two cases of a retropharyngeal space abscess due to the spread of an odontogenic infection. In all patients, early diagnosis was performed by computed tomography scanning and a physical examination. All patients were treated successfully by extensive surgical and antibiotic therapy.
Abscess ; Airway Obstruction ; Early Diagnosis ; Humans ; Lung Abscess ; Mediastinitis ; Pericarditis ; Pharynx ; Physical Examination ; Pleurisy ; Pneumonia, Aspiration

Progressive muscular dystrophy (PMD) is an X-linked recessive primary muscular disease characterized by progressive muscular weakness. It causes gait disturbance and complications such as pneumonia, heart failure, and aspiration, so lead to death. Becker muscular dystrophy (BMD) is a milder type of PMD, of which incidence is 5 cases per 100,000 populations. It begins later and evolves more slowly than Duchenne muscular dystrophy (DMD). In PMD patients without heart failure symptom, there may be ECG abnormality or ventricular dilatation, impaired ventricular function which is consistent with dilated cardiomyopathy, especially in DMD. In BMD, heart failure is rare but ECG or echocardiographic abnormality is often found. With the advance of molecular genetics, mutations of the dystrophin gene is proved to be related to the pathogenesis of PMD and dilated cardiomyopathy. We confirmed the deletion of exon 43-51 in the dystrophin gene a case of BMD with asymptomatic dilated cardiomyopathy, diagnosed by echocardiography.
Cardiomyopathy, Dilated ; Dilatation ; Dystrophin* ; Echocardiography ; Electrocardiography ; Exons* ; Gait ; Heart Failure ; Humans ; Incidence ; Molecular Biology ; Muscle Weakness ; Muscular Diseases ; Muscular Dystrophies ; Muscular Dystrophy, Duchenne* ; Pneumonia ; Ventricular Function

Progressive muscular dystrophy (PMD) is an X-linked recessive primary muscular disease characterized by progressive muscular weakness. It causes gait disturbance and complications such as pneumonia, heart failure, and aspiration, so lead to death. Becker muscular dystrophy (BMD) is a milder type of PMD, of which incidence is 5 cases per 100,000 populations. It begins later and evolves more slowly than Duchenne muscular dystrophy (DMD). In PMD patients without heart failure symptom, there may be ECG abnormality or ventricular dilatation, impaired ventricular function which is consistent with dilated cardiomyopathy, especially in DMD. In BMD, heart failure is rare but ECG or echocardiographic abnormality is often found. With the advance of molecular genetics, mutations of the dystrophin gene is proved to be related to the pathogenesis of PMD and dilated cardiomyopathy. We confirmed the deletion of exon 43-51 in the dystrophin gene a case of BMD with asymptomatic dilated cardiomyopathy, diagnosed by echocardiography.
Cardiomyopathy, Dilated ; Dilatation ; Dystrophin* ; Echocardiography ; Electrocardiography ; Exons* ; Gait ; Heart Failure ; Humans ; Incidence ; Molecular Biology ; Muscle Weakness ; Muscular Diseases ; Muscular Dystrophies ; Muscular Dystrophy, Duchenne* ; Pneumonia ; Ventricular Function

OBJECTIVE AND METHODS: To evaluate the effect of hypercholesterolemia on apoptosis (APOP) & proliferation (PROL) after vascular injury, we examined iliac arteries on 1, 3, 7 & 14 days after balloon injury (N=5 at each time) in rabbits with hypercholesterolemia (HC) and normocholesterolemia (NC). RESULTS: In media im-mediately after injury, APOP occurred massively & then decreased (TUNEL index=6.3+/-1.3 at D1, 0.9+/-0.7% at D14). HC did not affect early massive APOP but significantly (p<0.01) increased APOP, 3.3+/-1.5% at D14. Massive early APOP in media was followed by active PROL (PCNA index=6.0+/-3.3 at D7, 3.9+/-2.8% at D14). HC sustained the high activity of PROL upto D14 (8.9+/-2.7% at D14) (p<0.01). In intima where cells were scanty initially, PROL activity reached peak at D7 and then decreased (6.4+/-1.8% at D7, 2.5+/-1.8% at D14). HC significantly (p<0.05) enhanced PROL at D14 (5.8+/-2.2% at D14). In intima PROL was accompanied by low-grade APOP (1.3+/-1.1% at D7, 0.3+/-0.2% at D14). HC significantly (p<0.05) enhanced this low-grade APOP at D14 (0.9+/-0.4%). These effects of HC on APOP & PROL result in a significantly increased area of intima (0.4+/-0.2 in HC, 0.2+/-0.1 in NC) & media (0.5+/-0.1 in HC, 0.4+/-0.1 in NC) (p<0.01). Fundamental difference between HC & NC was infiltration of macrophage in HC, which was colocalized with APOP & PROL activities. CONCLUSIONS: Balloon injury induces early massive APOP followed by PROL in media, whereas in intima, it induces active PROL followed by low-grade APOP. Hypercholesterolemia does not affect early massive APOP, but enhances PROL & low-grade APOP at late phase, which results in intimal & medial hyperplasia.
Apoptosis* ; Cell Proliferation* ; Hypercholesterolemia* ; Hyperplasia ; Iliac Artery* ; Macrophages ; Rabbits ; Vascular System Injuries

OBJECTIVE AND METHODS: To evaluate the effect of hypercholesterolemia on apoptosis (APOP) & proliferation (PROL) after vascular injury, we examined iliac arteries on 1, 3, 7 & 14 days after balloon injury (N=5 at each time) in rabbits with hypercholesterolemia (HC) and normocholesterolemia (NC). RESULTS: In media im-mediately after injury, APOP occurred massively & then decreased (TUNEL index=6.3+/-1.3 at D1, 0.9+/-0.7% at D14). HC did not affect early massive APOP but significantly (p<0.01) increased APOP, 3.3+/-1.5% at D14. Massive early APOP in media was followed by active PROL (PCNA index=6.0+/-3.3 at D7, 3.9+/-2.8% at D14). HC sustained the high activity of PROL upto D14 (8.9+/-2.7% at D14) (p<0.01). In intima where cells were scanty initially, PROL activity reached peak at D7 and then decreased (6.4+/-1.8% at D7, 2.5+/-1.8% at D14). HC significantly (p<0.05) enhanced PROL at D14 (5.8+/-2.2% at D14). In intima PROL was accompanied by low-grade APOP (1.3+/-1.1% at D7, 0.3+/-0.2% at D14). HC significantly (p<0.05) enhanced this low-grade APOP at D14 (0.9+/-0.4%). These effects of HC on APOP & PROL result in a significantly increased area of intima (0.4+/-0.2 in HC, 0.2+/-0.1 in NC) & media (0.5+/-0.1 in HC, 0.4+/-0.1 in NC) (p<0.01). Fundamental difference between HC & NC was infiltration of macrophage in HC, which was colocalized with APOP & PROL activities. CONCLUSIONS: Balloon injury induces early massive APOP followed by PROL in media, whereas in intima, it induces active PROL followed by low-grade APOP. Hypercholesterolemia does not affect early massive APOP, but enhances PROL & low-grade APOP at late phase, which results in intimal & medial hyperplasia.
Apoptosis* ; Cell Proliferation* ; Hypercholesterolemia* ; Hyperplasia ; Iliac Artery* ; Macrophages ; Rabbits ; Vascular System Injuries