No abstract available.
Leiomyosarcoma*

Immunohistochemical study was performed for CEA staining patterns and PCNA indices. And the relationship between immunohistochemical findings and well-known clinical prognostic factors on the purpose of the clinical usefulness was evaluated. In forty seven cases of surgically removed colorectal carcinomas, the results were as follows; CEA staining patterns were apical (17 cases) and cytoplasmic (30 cases) type. Carcinomas with cyto plasmic pattern for CEA revealed more advanced Dukes' stage and more undifferentiated type and higher incidence of lymph node metastasis and were correlated with increased serum CEA levels. But PCNA indices showed no correlation with the Dukes' stage, histologic grade and CEA staining patterns. The cytoplasmic pattern of CEA immunohistochemistry may be a useful marker suggesting more aggressive biologic behavior of the colorectal carcinomas.
Colorectal Neoplasms* ; Cytoplasm ; Immunohistochemistry ; Incidence ; Lymph Nodes ; Neoplasm Metastasis ; Proliferating Cell Nuclear Antigen*

Genotoxic agents can induce various DNA lesions. DNA-Protein Crosslinks(DPCs) were known as the important DNA lesions which could impair gene expression because DPCs had a high probability of resisting repair and persisting through cell cycle. This repair resistance of DPCs could have biological significance but had not been evaluated clearly yet. Most of the studies that have evaluated the repair of DPCs only compared the extent of DPCs repair with other DNA lesions. We injected K2CrO4, a genotoxic agent, into Sprague-Dawley rats intraperitoneally(5mg/kg) and isolated blood lymphocytes 12 hours later. These lymphocytes were cultured in the mitogen added growth media and mitogen free media separately. The degree of the repair of DPCs was monitored for 4 days by the K-SDS assay. 4 day later, the amount of DPCs decreased by 4.6% in the mitogen added media but in creased by 10.9% in the mitogen free media. These results showed that DPCs induced by K2CrO4 were not repaired easily and the DPCs were biologically significant DNA lesions. We thought the decrease of DPCs in the mitogen added media was not due to the repair of DPCs, but from the increase of normal cell proliferation. Therefore, it is very important to consider the proliferation of normal cells when estimating the repair of DPCs.
Animals ; Cell Cycle ; Cell Proliferation ; DNA ; Gene Expression ; Lymphocytes* ; Rats* ; Rats, Sprague-Dawley

BACKGROUND: It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone cell metabolism remains unclear. It has been shown that thyroid hormones stimulate osteoclastic bone resorption indirectly via some unknown mediators secreted by osteoblasts, This study was undertaken to determine if interleukin-6 (IL-6) or interleukin-11 (IL-l1) could be the mediator (s) of thyroid hormone-induced bone loss. METHODS: We treated primary cultured human bone rnarrow stromal cells with 3,5,3-triiodo-thyronine (T) and measured basal and interleukin-l (IL-1)-stimulated IL-6/IL-ll production. We also investigated the possible modulating effect of 17B-estradiol (17B-E2.) on thyroid hormone action. RESULTS: T3 at 10 (-12) ~ 10 (-8) M concentration, significantly increased the basal IL-6 production in a dose-dependent manner, and also potentiated the stimulatory effect of IL-1 on IL-6 production. However, T failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treat#ment with l7B-E2. inhibited IL-1-stimulated IL-6 production, but the effects of T3 on IL-6 production were not affected by 17/B-E. CONCLUSION: These results suggest that thyroid hormone may increase bone resorption by increasing basal IL-6 production and potentiating IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects were independent of estrogen status.
Bone Marrow* ; Bone Resorption ; Estradiol ; Estrogens ; Humans* ; Interleukin-1 ; Interleukin-11* ; Interleukin-6* ; Mesenchymal Stromal Cells* ; Metabolism ; Osteoblasts ; Osteoclasts ; Osteoporosis ; Stromal Cells ; Thyroid Gland* ; Thyroid Hormones

No abstract available.
Actinomycosis*

No abstract available.
Actinomycosis*

This study was carried out to evaluate the cytotoxicity of rock wool fibers(RWFs) such as cell division disturbance, chromosomal and DNA damage, and mutagenicity using cultured cells. RWFs were the man made mineral fibers. In order to find the correlation between the cytotoxicity of RWFs and the phagocytic capacity of cells, the phagocytic processes were observed using scanning electron microscope. Cell division disturbance by RWFs was evaluated by the formation of multinucleated giant cells. The chromosomal damage was evaluated by the micronucleus formation. For the evaluation of oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine (8-OH-dG) formation was measured utilizing calf thymus DNA. Mutagenicity was determined by the point mutation of HGPRT and the effect of RWFs on cell transformation was also observed. 1. Compared with the results of chrysotile, RWFs were no or little effect on the cell growth according to the results done by the tests of cell proliferation inhibition and relative plating efficiency. 2. The frequency of multinucleated giant cell formation was increased by the treatment of RWFs and it was dose-dependent. However, the effect of RWFs was weaker than that of chrysotile. 3. The number of micronuclei formed in the RWFs treated cells was between those of cells treated with chrysotile and those of untreated cells. 4. The 2 fold increase in the formation of 8-OH-dG in calf thymus DNA was observed in the cells treated with RWFs in the presence of H2O2. On the other hand, chrysotile had no effect on the 8-OH-dG formation. 5. RWFs had no effect on the HGPRT point mutation and cell transformation. These results showed that RWFs could induce chromosomal damage, cell division disturbance and oxidative DNA damage in the RWFs treated cells.
Asbestos, Serpentine ; Cell Division ; Cell Proliferation ; Cells, Cultured ; DNA ; DNA Damage ; Giant Cells ; Hand ; Hypoxanthine Phosphoribosyltransferase ; Mineral Fibers ; Point Mutation ; Thymus Gland ; Wool*

Glycogen storage diseases(GSD) are inherited disorders affecting glycogen metabolism and type I GSD is due to the absence or deficiency of glucose-6-phosphatase(G6Pase) enzyme in the liver, kidney, and intestinal mucosa. The defect leads to inadequate hepatic conversion of G6P to glucose and thus make affected individuals susceptible to fasting hypoglycemia, and the accumulation of glycogen occurs in the liver and other organs. Type Ia is the most common form of GSD and clinically growth retardation may manifest of GSD itself rather than growth hormone deficiency(GHD), but we experienced a case of type I GSD with GHD in a 14-year-o1d male. The height was 125 cm, compatible with 50 th percentile of height of 8 years of age. He has doll-like face with fat cheek, relatively thin extremities, and metabolic acidosis, hyperuricemia, hypoglycemia, hyperlipidemia. GH stimulation test with clonidine and L-dopa revealed that the patient had decreased GH secretion. After laboratory work up including liver biopsy, he was diagnosed as type I GSD. Hypoglycemia was managed with frequent feeding with high starch diet(uncooked cornstarch). Metabolic acidosis and hyperuricemia were treated with sodium bicarbonate, allopurinol and probenecid. The patient is being followed at out-patient clinic with clinical improvement after of diet therapy and GH administration.
Acidosis ; Allopurinol ; Biopsy ; Cheek ; Clonidine ; Diet Therapy ; Extremities ; Glucose ; Glycogen Storage Disease* ; Glycogen* ; Growth Hormone* ; Humans ; Hyperlipidemias ; Hyperuricemia ; Hypoglycemia ; Intestinal Mucosa ; Kidney ; Levodopa ; Liver ; Male ; Metabolism ; Outpatients ; Probenecid ; Sodium Bicarbonate ; Starch

The ultrastructural changes of sciatic nerve and immunohistochemical changes of beta-catenin, PCNA, substance P were studied at the proximal segment of rat sciatic nerve after compression injury. We used 90 Sprague Dawley rats and the sciatic nerve compressed using silicon tube. We divided experimental groups which were the compression group for 1 hour (1C), for 2 hours (2C), and for 3 hours (3C), the release group for 1 day (1C1R) and 3 days (1C3R) after the compression for 1 hour, the release group for 1 day (2C1R) and 3 days (2C3R) after the compression for 2 hours, the release group for 1 day (3C1R) and 3 days (3C3R) after the compression for 3 hours. The rats were sacrified and took the sciatic nerve specimen. The specimens were investigated under the light microscope after hematoxylin & eosin, toluidin blue, and immunohistochemical stainings. In the H & E finding, the axon of the 1C disappeared, but recovered at the 1C3R. The part of nerve fibers at the 2C were swollen, but began to be partially recovered at 2C3R. Most nerve fibers were enlarged at the 3C, but markedly decreased at the 3C1R. The beta-catenin reaction disappeared at the 1C, but almost recovered at the 1C3R. This reaction of the 2C disappeared in the large fibers, but began to be recovered in the small fibers at the 2C1R. This reaction of the 3C disappeared in the large fibers, but began to be recovered at the 3C1R and 3C3R. The PCNA reaction prominently appeared at the 1C3R and 2C3R, the more prominent reaction at the 3C1R, and markedly increased reaction at the 3C3R. The substance P reaction of the 1C1R was mild positive, and the 2C1R and 3C1R were strong positive. In the toluidin blue staining, the myelin sheaths near the perineurium began to be thickened at the 1C, but almost recovered at the 1C3R. Many myelin sheaths became to be very thickened at the 2C and 3C, but almost recovered at the 2C3R and 3C3R. In the electron microscopic findings, the myelin sheaths of the 1C underwent the demyelination with the separated lamellae and the increase microtubules. At the 1C3R, the axolemma was attached on the myelin sheath and the axon was recovered. the myelin sheaths of the 2C underwent the demyelination with the separated axolemma. At the 2C1R, the myelin sheath was recovered by the developing Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. At the 2C3R, the myelin sheath tended to be recovered by the increased rough endoplasmic reticulum and mitochondria of Schwann cells, many intraaxonal mitochondria of demyelinated nerve fibers. The myelin sheaths of the 3C began to be underwent severe demyelination from the middle portion of the sheath and the vacuolization of intraaxonal mitochondria. At the 3C1R, the myelin sheaths were recovered and contained many extended microtubules, mitochondria, and small granules. At the 3C3R, severe demyelinated nerve fibers were recovered by increasing microtubules. The proximal retrograde degeneration of sciatic nerve by the acute compression appeared the loss of the axons and the swelling of nerve fibers. The beta-catenin reaction was disappeared by the compression, but recovered by releasing. This reaction may be played a important role of the recover of demyelination. The PCNA reaction of Schwann cells was increased by the nerve compression. In the substance P finding, the pain after the compression appeared at the 1 day after releasing. Electron microscopic changes after sciatic nerve compression were the demyelination, the separated lamellae and the increase of intraaxonal microtubules. After releasing, the nerve fibers were recovered by developing Schwann cell, the intraaxonal mitochondria, and the transported granules through extending microtubules.
Animals ; Axons ; beta Catenin* ; Demyelinating Diseases ; Endoplasmic Reticulum, Rough ; Eosine Yellowish-(YS) ; Hematoxylin ; Microtubules ; Mitochondria ; Myelin Sheath ; Nerve Fibers ; Peripheral Nerves* ; Proliferating Cell Nuclear Antigen* ; Rats* ; Rats, Sprague-Dawley ; Retrograde Degeneration ; Schwann Cells ; Sciatic Nerve ; Silicones ; Substance P*

Autonomic dysreflexia is a syndrome characterized by severe hypertension, headache, sweating that is seen in spinal cord injury population. It can be a life-threatening problem if not promptly recognized and treated. Since the most common cause is bladder distention, it is essential that the urologist sh6fild be familiar with this syndrome. Two hundred ninety four patients with spinal cord injury were reviewed for the prevalence rate and clinical manifestations of autonomic dysreflexia. The time of onset post-injury, precipitating causes, presenting symptoms and management were analyzed. 42 patients (34.4%) of 122 patients with lesion above T6 level exhibited autonomic dysreflexia. The majority of patients (61.9%) had manifested signs and symptoms of autonomic dysreflexia within the first year. The precipitating causes were bladder distention (69.0%), bowel distention (23.8%) and urinary tract infection (7.1%). The presenting symptoms of autonomic dysreflexia were headache (88.1%), sweating (88.1%), hot flushing (28.6%), chest discomfort, hyperpnea and spasm. The management of autonomic dysreflexia include prompt bladder erupting, bed rest and appropriate bowel preparation. In conclusion, prompt recognition and appropriate management of autonomic dysreflexia are essential to prevent life-threatening sequelae.
Autonomic Dysreflexia* ; Bed Rest ; Flushing ; Headache ; Humans ; Hypertension ; Prevalence ; Spasm ; Spinal Cord Injuries* ; Spinal Cord* ; Sweat ; Sweating ; Thorax ; Urinary Bladder ; Urinary Tract Infections