No abstract available.
Carcinoma, Papillary* ; Thyroid Gland*

No abstract available.
Multiple Endocrine Neoplasia*

No abstract available.
Graves Disease* ; Humans ; Thyroid Gland*

No abstract available.
Hernia* ; Pneumoperitoneum*

No abstract available.
Humans ; Rhinitis* ; Skin Tests* ; Skin*

No abstract available.
Keratins*

We managed 118 patients with benign prostatic hyperplasia by transurethral resection during January 1994 and December 1995 in Eul Ji Medical Center and all patients were operated upon by 2 staff doctors. Among 118 cases, 7 cases with intraoperative complications such as bladder injury or severe prostatic capsule injury and 8 cases with combined neuropathic bladder or chronic urinary retention and 2 cases with urethral stricture were excluded. The average age of 101 cases were 66.4 years old (50-92), and average weight of resected adenoma was 10.0 gm (2-32). We categorized these patients randomly into 2 groups. In group I (n=48), we removed the urethral catheter within 2 days after TURP and in group II (n=53), we removed it after 3 days (mean 4.2 days) following surgery. The average hospital stay postoperatively was4.1 days in group I and 7.4 days in group II. Recatheterization rate was 8.3% (4/48) in group I and 5.6% (3/53) in group II (p>0.05). There was no statistical difference in other complication including failure to void, intraoperative bleeding, urethral stricture, incontinence and TUR syndrome. This study supports early catheter removal after TURP would become an accepted and routine postsurgical practice following uncomplicated TURP.
Adenoma ; Catheters* ; Hemorrhage ; Humans ; Intraoperative Complications ; Length of Stay ; Prospective Studies* ; Prostatic Hyperplasia ; Transurethral Resection of Prostate* ; Urethral Stricture ; Urinary Bladder ; Urinary Bladder, Neurogenic ; Urinary Catheters ; Urinary Retention

Oncogenes are known to be involved in normal cellular growth and proliferation as well as in carcinogenesis. It is reported that stimulation of quiescent cells with growth factors makes the oncogenes produce protein products as an early and immediate response, and these protein products induce or control the cell growth. Among those oncogenes, c-fos and c-myc are well known for its generalized expressions. An experiment was performed in order to prove the hypothesis that oncogene expressions would have the same pattern with that of cellular growth by growth factors in cultured normal rat thyroid cell line(FRTL-5). Ribonucleic acids of FRTL-5 cells were extracted time-sequentially at 15, 30, 60 and 120 minutes after administration of growth factors to the media of quiescent FRTL-5 cells. Extracted ribonucleic acids were blotted to the nitrocellulose membrane, and then hybridized with radiolabelled c-fos and c-myc oligonucleotide probes, and -actin probes. Hybridized dot blots on nitrocellulose membrane were autoradiographed on X-ray films, and the amount of radioactivity were measured by densitometry. Densitometric readings were used as the indices of oncogene expressions. The concentrations of TSH, IGF-I and IgG from patients with Graves' disease, which showed the maximum expressions of c-fos and c-myc in quiescent FRTL-5 cells, were TSH 10 mU/ml, IGF-I 100 ng/ml and IgG from patients with Graves' disease 1 mg/ml, respectively. Expressions of c-fos and c-myc were more prominent in combined administrations of TSH and IGF-I, or IgG from patients with Graves' disease and IGF-I than in case of TSH and IgG from patients with Graves' disease. IgG from patients with primary myxedema suppressed oncogene expressions provoked by TSH or IgG from patients with Graves' disease, but not by IGF-I. Expressions of c-fos and c-myc were more prominent by the combined administration of TSH with TPA which stimulated the phosphoinositide turnover-protein kinase C-calcium system than by those of TSH with dBcAMP, forskolin, IBMX or cholera toxin which stimulated adenylate cyclase system. From the above results, following conclusions were obtained. 1) Expressions of c-fos and c-myc by growth factors have similar patterns with those of cell growth by growth factors in FRTL-5 cells. 2) It is suggested that the actions of TSH and IgG from patients with Graves' disease would be manifested through the same signal transduction system, and that of IGF-I would be manifested through its own, but the oncogenes would be expressed mainly through adenylate cyclase system.
1-Methyl-3-isobutylxanthine ; Adenylyl Cyclases ; Animals ; Bucladesine ; Carcinogenesis ; Cell Line* ; Cholera Toxin ; Colforsin ; Collodion ; Densitometry ; Genes, myc* ; Graves Disease ; Humans ; Immunoglobulin G ; Insulin-Like Growth Factor I ; Intercellular Signaling Peptides and Proteins* ; Membranes ; Myxedema ; Oligonucleotide Probes ; Oncogenes ; Phosphotransferases ; Radioactivity ; Rats* ; Reading ; RNA ; Signal Transduction ; Thyroid Gland* ; X-Ray Film

Nine cases of primary localized cutaneous amyloidosis were studied by immunoperoxidase technique (ABC method) employing anti-keratin antibodies. All specimens were examined using consecutive paraffin sections to confirm the correspondence between amyloid existing area and reactive sites. Anti-keratin antibody 34pE which recognize 68, 58, 56.5, 56kd keratin peptides reacted with amyloid deposits in both lichen amyloidosus and macular amyloidosis. However, anti-keratin antibodies 34pB4 and 35pH did not react with amyloids. In general, Dylon staining positive material, keratin reacted with 34pE and amyloid P showed similar distribution in serial sections, but did not show the same one. Several keratin bodies reacted with 34pE, which were not stained with Dylon staining or antiamyloid P were found in the dermis of one specimen. These results suggest that immunohistochemical staining with antikeratin antibody 34pE using formalin-fixed, paraffin-embedded sections appeared to be a useful method in studying the histogenesis of primary localized cutaneous arnyloidosis.
Amyloid* ; Amyloidosis* ; Antibodies* ; Catalytic Domain ; Dermis ; Immunoenzyme Techniques ; Lichens ; Paraffin ; Peptides ; Plaque, Amyloid*

No abstract available.
Budd-Chiari Syndrome ; Humans