Transient cerebral ischemia was induced by bilateral common carotid artery ligation with reperfusion to understand its effect on the expression of NMDA receptor subunits 2A (NR2A), 2B (NR2B), and NF200 The changes of the expressions of NR2A, NR2B, and NF200 in cerebral postsynaptic density (PSD) were evaluated through immunoblot analyses. The expressions of NR2A and NF200 were markedly decreased until 18 hours after reperfusion, while that of NR2B was increased. The immunohistochemistry with NFIGO antibody showed that NF200 protein, which is a marker for neuronal damage, was also significantly decreased at this time point indicating neuronal damages, and the morphological damages of neuronal cells were evident by hyperchromatic condensation of nucleus, irregular cell membrane, displacement of nucleus, and chromatolysis of Nissl substances in toluidine blue stain. However, from 18 hours to 3 day after reperfusion, immunoblot analyses showed that NF200 was increased significantly, while the expression of NR2A were recovered to the control level and that of NR2B was returned to somewhat higher level than control. The NR1/NR2B-type receptor is known to have a longer offset decay time than NR1/NR2A-type ones, and to be more potent in Ca2 influxing. Therefore, our results suggest that, until 18 hours, neurons are damaged by overinflux of Ca2 through NR1/NR2B receptors which helps to degrade NF200 by Ca2 sensitive professes resulting in damages to intracellular transport. The fact that the expression of NF200 was increased even though the NR2A and NR2B are control level during 18 hours to 3 days after damage suggests that NMDA receptor subunits expressed at this time may not form functional receptors. The worsening of some neuronal damages after 3 days may indicate that an abnormal reorganization of elevated NF200 between 18 hours to 3 days further disturb intracellular transport and functions of cell membrane which cause cell death.
Animals ; Carotid Artery, Common ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Immunohistochemistry ; Ischemic Attack, Transient* ; Ligation ; N-Methylaspartate* ; Neurons ; Post-Synaptic Density ; Rats* ; Reperfusion ; Tolonium Chloride

In the rat brain, partial ischemia causes a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulaly NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Calcium-activated protease calpain, excessive degradation of MAP-2, together with the calpain-sensitive microtubule and neurofilaments, would be expected to disrupt intracellular transport- and membrane-related functions that is vital to neurons. Changed of NR subunit 2A, 2B, MAP2 and NF200 in rat hippncampal postsynaptic density[PSD] after partial ischemic injury were investigated though immunoblot analyses. To understand the effect of Ca2+, influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and routine staining method. We found that immunoreactivity to NR2B receptor subuit in the hippocampal formation PSD was upregulated while MAP2 and NF200 was down-regulted at 18 hours after initial partial ischemic insult. On the other hand, morphological changes of neuronal cell in partial ischemic conditions were manifested as eosinophilic inclusion bodies in the cytoplasm which is progression of neuronal damage after 6 days. Calcium influx through NR1/NR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which cause neuronal cell death.
Animals ; Brain ; Calcium ; Calpain ; Cell Death ; Cell Membrane ; Cytoplasm ; Cytoskeleton ; Eosinophils ; Hand ; Hippocampus* ; Immunohistochemistry ; Inclusion Bodies ; Ischemia ; Microtubules ; N-Methylaspartate ; Neurons ; Pathology ; Peptide Hydrolases ; Proteolysis* ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate

No abstract available.
Knee* ; Ligaments*

In the rat brain, global hypoxia cause a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulary NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Changes of NR subunit 2B, MAP2 and NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and H & E staining. We found that immunoreactivity to NR2B antibody in the cerebral cortex PSD was up-regulated while MAP2 and NF200 was down-regulated at 30 hours after initial hypoxic insult. At this time, morphological changes of neuronal cells in hypoxic conditions were manifested as down-regulation of MAP2 and NF200 immunoreactivities, hyperchromatic condensation of cytoplasm and nucleus, homogenizing cell change, expansion of perineuronal space and dispersion of chromatin. From 3 days, NR2B, MAP2, NF200 were up-regulated simultaneously. On the other hand, morphological alterations in hypoxic neurons were progress further. Our present results suggests that Calcium influx through NR1/NR2B receptor channel is effective whithin 30 hours but ineffective from 30 hours. Delayed neuronal cell death triggered by Ca2+ influx through NR1/NR2B receptor channel within 30 hours, which may activate intracellular profeases. Proteolysis of cytoskeleton by activated protease leads to its abnormal reorganization and eventually damages normal function of cell membrane which causes neuronal cell death.
Animals ; Anoxia ; Brain ; Calcium ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Chromatin ; Cytoplasm ; Cytoskeleton* ; Down-Regulation ; Hand ; Immunohistochemistry ; N-Methylaspartate* ; Neurons ; Pathology ; Proteolysis ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; Up-Regulation*

The fatty hamartoma of pericardium is characterized by abnormal accumulations of adipose tissue forming a recognizable mass. We reported a case that could best be put into "fatty hamartoma" group. This 66 year old male presented with atrial fibrillation came in for a anterior mediastinal mass. He received an operation for adenocarcinoma of ascending colon several months ago. The chest CT revealed an inhomogeneous mass in the right anterior mediastinal area, which was not clearly demarcated from the right cardiac border. The heart was deviated to the left side due to the mass. Surgical excision was performed under the impression of cardiac teratoma. The large mass was well encapsulated, and was bright yellow and partly pink, and measured 12x8 cm. Microscopically, the mass consisted predominantly of mature fat cells and abundant fibrous tissue with scattered nests of primitive cardiac muscle cells. Reviewing the literature we found the term "fatty hamartoma" could also refer to rhabdomyolipoma or fibrolipoma. Since it contains entrapped cardiac muscle cells, abundant fibrous tissue, multiple blood vessels and fetal fat cells, it could best the categorized into "hamartoma". The term "fatty" represents it's main component. Therefore we propose the term "fatty hamartoma" that could to be used further.
Male ; Humans ; Adenocarcinoma ; Hamartoma

This case report draws attention to the possibility of symptomatic and asymptomatic intraarticular ganglion cyst which was situated adjacent to the insertion sites of the anterior or posterior cruciate ligament. In many reports and our case, MR imaging is recommended as the modality of choice in diagnosing method and the cyst, if encountered, is successfully treated with arthroscopie technique. We report one case of symptematic ganglion cyst of the posterior cruciate ligament with review of literatures.
Ganglion Cysts* ; Knee ; Magnetic Resonance Imaging ; Posterior Cruciate Ligament*

Genes of cancer-associated testis antigens (CTAs) are expressed in various cancer tissues. In order to use CTAs as cancer diagnosis marker, we developed molecular method for detection of CTAs transcripts in tissue. In order to know the applicability of DNA of cancer-associated testis antigens (CTAs) on cancer diagnosis, molecular diagnostic methods for detection of gene expression of melanoma antigen gene (MAGE), GAGE, and B melanoma antigen (BAGE) was studied. After comparing DNA sequences of CTAs, S1/AS1 and S2/AS2, GAGE-S/ GAGE-AS, and BAGE-S/BAGE-AS primers were designed for the detection of MAGEs, GAGEs and BAGEs, respectively. The gene expression of CTAs in cancer cell lines, head and neck cancer tissues, ovary cancer tissue, and peritoneal cells of gastric cancer patients were investigated by reverse transcription-polymerase chain reaction (RT-PCR) using these primers. The MAGEs, GAGEs and BAGE genes were expressed in 8/8 (100%), 5/8 (62.5%) and 1/8 (12.5%) of head and neck cancer tissues, respectively. The gene expression of MAGEs were also detected in 8/10 (80%) of ovary cancer tissues and in 9/10 (90%) of peritoneal cells of gastric cancer patients in RT-PCR test using S1/AS1 primers. The results of this study suggest that molecular diagnosis method using CTAs genes, especially RT-PCR using S1/AS1 primer combination, is useful for diagnosis of cancer and it will be used for the prediction of cancer progression or regression and metastasis in future.
Base Sequence ; Cell Line ; Diagnosis* ; DNA ; Gene Expression ; Head and Neck Neoplasms ; Humans ; Melanoma ; Neoplasm Metastasis ; Ovarian Neoplasms ; Pathology, Molecular ; Stomach Neoplasms ; Testis*

Spondylometaphyseal dysplasia (SMD) is an extremely rare, which affects the spine and metaphy-ses of the tubular bones on terms of enchondrogenesis. Children who had Kozlowski dwarfism, type of SMD are not recognized until they reach school age since they have normal clinical feature, weight and size in early childhood. Authors experienced a typical case of Kozlowski type of SMD in a 10 years old male who had i) generalized platyspondyly with anterior tapering of vertebrae ii) generalized metaphyseal dysplasia iii) minimal changes in the carpal and tarsal bones. This case is to be reported with review of references.
Child ; Dwarfism ; Humans ; Male ; Spine ; Tarsal Bones

No abstract available.
Prevalence* ; Ulsan*

Fat embolism is the presence of fat globules in the peripheral circulation and in the lung, brain, kidney, heart, and so on -not in the fine emulsion of a metabolic lipemia but in globules large enough to obstruct arterioles and capillaries. The fat droplets can derive from fractures of long bone due to disruption of the fatty marrow, from extensive bruising of the soft tissue, and from fat tissue in burns. Fat embolism has also been reported in patients suffering from various diseases including alcoholism, fatty liver, diabetes mellitus and pancreatitis. We investigated 19 autopsies with fatty liver of varying degrees to establish a correlation between fatty change of liver and pulmonary fat embolism. Among 19 cases, 3 cases with moderate to severe fatty change of liver, and 1 case with submassive hepatic necrosis and mild fatty change showed Grade II pulmonary fat embolism. In histologic section with Sudan III stain, the arteries and capillaries of lung were occupied and distended by round, oval, or staghorn fat globules. The alveoli may contain edema fluid and blood. Although the pulmonary fat embolism occuring in the presented cases didn't cause death on its own, one should be aware that a life-threatening mobilization of fat into the lungs and even into the systemic circulation is possible in fatty liver and submassive hepatic necrosis.
Alcoholism ; Arteries ; Arterioles ; Autopsy ; Bone Marrow ; Brain ; Burns ; Capillaries ; Diabetes Mellitus ; Edema ; Embolism, Fat* ; Fatty Liver* ; Heart ; Humans ; Hyperlipidemias ; Kidney ; Liver ; Lung ; Necrosis ; Pancreatitis ; Sudan