We present a case of carcinoma erysipelatoides which or iginated from an internal organ. The patient was a 50 year-old female who had peritoneal carcinomatosis, She presented an erythematous lesion resembling erysipelas on her right breast. Histopathologic findings were consistent with metastatic adenocarcinoma but clinically it was not associated with carcinoma of the breast.
Adenocarcinoma ; Breast ; Carcinoma ; Erysipelas ; Female ; Humans ; Middle Aged

The present study was carried out to find a simple and safe in. vitro test for phtotoxic drugs. Authors selected two strains of Salmonella typhimurium(TA98 and TA102) which have been used in Ames test for the detsction of mutagenecity af various chemical substances. Both strains are genuine products of genetic enzineering. The etrain TA98 should be highly vulnerable to ultraviolet radition because it lacks normal I)NA excision repair gene. The strain TA102 was chosen as control since it maintained the DNA repair gene. These strains were subjected to increasing dosea of UVA with or without pretreatment of 8 methoxypsoralsn(8-MOP) which is a prototype of photatoxic druge. The authors made use of a perforated stain-less steel template which provided a simple and eosy monitoring of ultraviolet irradiation effects i.e. clear zones due to inhibition of the atrains could be determined. By using this methad, the authors acquired the following results .' I. 8-MOP alone exerted no inhibition on both strains at concentration upto 100mg /ml. 2. UVA irradiation alone showed no growth inhibition at dose upto 5J/cm. 3. UVA irradiation after pretreatment with 8 MOP resulted varying growth inhibition in proportion to irradiation doses. 4. Authors found a suitable concentration of 8-MOP for this test is 10pg/ml. With this ccncentrstion, minimal phatatoxic dose of UVA were O.l J/cm for the strain TA98 and 1.0J/cm for the strain TA102 respectively.
Dermatitis, Phototoxic ; DNA Repair ; Methoxsalen ; Salmonella ; Steel

Herein we report a 51-year-old male with angioimmunoblastic lymphadenopathy who had developed rnaculopapular eruptions after the administration of crystalline penicillin, acetylsalicylic acid and sulpyrine. Skin biopsy showed mild lyrnphohistiocytic infiltration and extravasated RBCs around the blood vessels in the upper dermis. He had run a progressively downhill course in spite of vigorous chemotherapy and ultimately died.
Aspirin ; Biopsy ; Blood Vessels ; Crystallins ; Dermis ; Dipyrone ; Drug Therapy ; Humans ; Immunoblastic Lymphadenopathy ; Lymphatic Diseases* ; Male ; Middle Aged ; Penicillins ; Skin

No abstract available.
Glycoproteins* ; Immunity, Cellular ; Klebsiella pneumoniae* ; Klebsiella*

No abstract available.
Biopsy* ; Prostate*

A 21-year-old male suffered from generalized anhidrosis and heat intolerance for about 15 years. Other clinical features included multiple angiokeratoma on the back, scrotum and extremities, together with ocular involvement. The electronmicroscopic studies of the skin demonstrated laminated intracytoplamic inclusions in the endothelial cells, pericytes of dermal vessels, fibroblasts and eccrine glandular cells. a Galactosidase assay of leukocytes from the patient and his uncle showed nearly absence of the activity,
Angiokeratoma ; Endothelial Cells ; Extremities ; Fibroblasts ; Galactosidases ; Hot Temperature ; Humans ; Hypohidrosis* ; Leukocytes ; Male ; Pericytes ; Scrotum ; Skin ; Young Adult

Posteroanterior radiographs of normal wrist were taken in seventeen volunteers, and analysed to determine the dynamic relationships between the radiocarpal and midcarpal joint during radioulnar deviation. The total arc of radioulnar deviation was 59 degrees, and the motion was 44% radiocarpal and 56% midcarpal. During radioulnar deviation, the motion at the midcarpal joint was more than that at the radiocarpal joint. It is suggested thst dorsoradial and palmar-ulnar flexion as it occurs at the midcarpal joint can be correlated in radio-ulnar deviation of the wrist more than the coronal sliding motions as it occurs mainly at the radiocarpal joint.
Joints ; Volunteers ; Wrist

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*

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