No abstract available.
Cholangitis*

CT is a valuable diagnostic modality in evaluation of bladder injury, extension of paravesical hematoma, pelvic bone fracture or injury of adjacent soft tissue although the diagnostic accuracy of bladder injury itself is lower than that of retrograde cystography. We analized CT findings in thirty cases of bladder injury or paravesical hematoma due to blunt lower abdominal or pelvic trauma and compared them with operation fildings in eight cases. IVP in eight cases and cystography in fifteen cases. The types of bladder injury were classified as contusion, intraperitoneal bladder rupture, extraperitoneal bladder rupture and combined rupture. The locations of paravesical hematoma were classified as perivesical, prevesical or combined. There was no close relationship between the types of pelvic bone fracture and distribution of paravesical hematoma. The paravesical hematomas in fifteen patients without bladder injury were located in prevesical space only. Perivesical hematomas were noted in nine of fifteen patients with bladder injury and were not noted in patients without bladder injury. Thus, we concluded that the presence of perivesical hematoma on CT is a diagnostic sign of bladder injury even though extravasation of contrast from the bladder is not identified, and if there is extraperitoneal hematoma, possibility of bladder injury or other pelvic trauma should be considered.
Contusions ; Hematoma ; Humans ; Pelvic Bones ; Rupture ; Urinary Bladder

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*

We have recently experienced a rare case of abdominal aortic injury caused by shearing force falling from 8 meter height in upright position. The patient was 43 year old and sustained Ll, L2, L5, compression fractures and both distal tibia and fibula comminuted fractures involving ankle joints. 2 years and 2 months later, marked stenosis of the distal abdominal aorta was found together with clinical manifestations of ischemia of both legs. Aorto-femoral bypass on both sides has completely relieved the symptoms.
Accidental Falls ; Ankle Joint ; Aorta, Abdominal ; Constriction, Pathologic ; Fibula ; Fractures, Comminuted ; Fractures, Compression ; Humans ; Ischemia ; Leg ; Tibia

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

Growth under conditions of iron-restriction and the production of siderophore was examined in Vibrio mimicus ATCC 33653. This strain grew and multiplied in the presence of the high-affinity iron chelators ethylenediamine-di (o-hydroxyphenylacetic acid). Chrorne azurol S (CAS) agar and solution were used to detect the production of siderophore under these condition. Siderophore could be detected in the iron-rcstricted culture supernatants. The siderophore was extracted from iron-restricted culture supernatants by phenol-chloroform-ether method and purified by Dowex ion-exchange and Sephadex G-25 gel filtracton chromatography. The purified siderophore was confirmed by paper chromatography and HPLC. The Purified siderophore enhanced the growth of V. mimicus when the bacterium was grown in iron limited medium. Injection of both the siderohore and the bacteria to mice resulted in more rapid death than that of the only bacteria. However, the siderophore did not show lethality to mice and any toxicity to cell line like HeLa and U937.
Agar ; Animals ; Bacteria ; Cell Line ; Chelating Agents ; Chromatography ; Chromatography, High Pressure Liquid ; Chromatography, Paper ; Iron ; Mice ; Vibrio mimicus* ; Vibrio*

No abstract available.
Immunoglobulin G* ; Influenza, Human*

No abstract available.
Pregnancy, Heterotopic*

We experienced a case of congenital rubella syndrome manifesting patent ductus arteriosus, petechiae, microcephaly, intrauterine growth retardation, and hepatomegaly in one-day-old female newborn infant. Congenital rubella syndrome was confirmed by positive results of anti-rubella IgM in the sera of patient. Anti-rubella IgM was negative in the sera of mother, while anti-rubella IgG was positive.
Ductus Arteriosus, Patent ; Female ; Fetal Growth Retardation ; Hepatomegaly ; Humans ; Immunoglobulin G ; Immunoglobulin M ; Infant, Newborn ; Microcephaly ; Mothers ; Purpura ; Rubella Syndrome, Congenital*