No abstract available.
Exostoses*

Arterial restenosis frequently develops after open or endovascular surgery due to intimal hyperplasia. Since tissue transglutaminase (TG2) is known to involve in fibrosis, wound healing, and extracellular matrix remodeling, we examined the role of TG2 in the process of intimal hyperplasia using TG2-null mice. The neointimal formation was compared between TG2-null and wild-type (C57BL/6) mice by two different injury models; carotid ligation and carotid loop injury. In ligation model, there was no difference in intimal thickness between two groups. In loop injury model, intimal hyperplasia developed in both groups and the intimal/medial area ratio was significantly reduced in TG2-null mice (P = 0.007). TG2 was intensely stained in neointimal cells in 2 weeks. In situ activity of TG2 in the injured arteries steadily increased until 4 weeks compared to uninjured arteries. Taken together, intimal hyperplasia was significantly reduced in TG2-null mice, indicating that TG2 has an important role in the development of intimal hyperplasia. This suggests that TG2 may be a novel target to prevent the arterial restenosis after vascular surgery.
Animals ; Carotid Arteries/pathology/*surgery ; Disease Models, Animal ; GTP-Binding Proteins/deficiency/genetics/*metabolism ; Hyperplasia ; Mice ; Mice, Inbred C57BL ; Transglutaminases/deficiency/genetics/*metabolism ; Tunica Intima/*pathology

Endometriosis is defined as the presence of functional endometrial tissue in an ectopic site. The incidence of endometriosis is from 10% to 20% for women of reproductive age. From 1% to 2% of woman with endometriosis have urinary tract lesions, of which from 70% to 80% involve the bladder. Yet ureteral endometriosis is very uncommon, and it is noted in only 0.1% to 0.4% of these cases. We report here on one case of ureteral endometriosis.
Endometriosis* ; Female ; Humans ; Incidence ; Ureter* ; Ureteral Obstruction ; Urinary Bladder ; Urinary Tract

No abstract available.
Female* ; Humans ; Transplants*

No abstract available.
Teratoma* ; Turner Syndrome*

Endometriosis is defined as an extrauterine growth of endometrial tissue and it is primarily limited in the pelvis but it can also occur in the pleural cavity as well as pulmonary parenchyme. The diagnosis of pulmonary endometriosis is usually based on the clinical history of recurrent hemoptysis in association with menstrual cycle and by histopathologic confirmation of endometrial tissue in the lung parenchyme. Pulmonary endometriosis was first reported by Lattes in 1956, and dozens of cases have been reported so far. We experienced a case of 25 year old single woman with a history of hemoptysis in association with her menstruation. The bleeding focus was localized with chest CT scan and repeated fibrooptic bronchoscopy and basal segmentectomy of the right lower lobe was performed. The resected specimen shows endometrial stroma and glands of early proliferative phase with respiratory epithelium on the laterobasal bronchus. Her postoperative course was uneventful with no recurrence of hemoptysis during 6 months of follow-up in the outpatient clinic.
Adult ; Ambulatory Care Facilities ; Bronchi ; Bronchoscopy ; Diagnosis ; Endometriosis* ; Female ; Follow-Up Studies ; Hemoptysis ; Hemorrhage ; Humans ; Lung ; Mastectomy, Segmental ; Menstrual Cycle ; Menstruation ; Pelvis ; Pleural Cavity ; Recurrence ; Respiratory Mucosa ; Tomography, X-Ray Computed

PURPOSE: Unilateral ureteral obstruction(UUO), a well established experimental model of renal injury, gives rise to tubulointerstitial fibrosis, tubular dilatation and cellular atrophy. Angiotensin(ANG) II may take the prime role in the regulation of this response. The objectives in the current investigation were to determine whether the renal response to UUO involves the dedifferentiation of tubular epithelial cells to mesenchymal cells(expressing vimentin, V) whether the response implicates the transformation of fibroblasts to myofibroblasts(expressing alpha-smooth muscle actin, SMA), and whether these responses depend on the action of ANG II or not. METHODS: Unilateral ureteral ligation and sham operations were performed in 12 adult male Sprague-Dawley rats. An additional 18 rats received exogenous ANG II at 50 ng/min or vehicle for one week using an osmotic minipump inserted into the interscapular area. Rats were sacrificed on postoperative day seven or day 14. To know the expression of vimentin(V) and alpha-smooth muscle actin (SMA) proteins, immunohistochemical staining and Western blot assay were done. RESULTS: In immunohistochemical staining, following UUO, V-positive cells appeared markedly in the interstitium and tubular cells within dilated tubules. UUO also markedly increased alpha-SMA expression in the interstitium surrounding dilated tubules. In Western blotting, UUO increased V(five times of Sham) and alpha-SMA(2.5 times of Sham) expression. ANG II infusion increased alpha-SMA significantly(two times of control), but not V expression in Western blotting. CONCLUSION: Phenotypic transformation of fibroblasts to myofibroblasts following UUO may depend on ANG II, but dedifferentiation of tubular epithelial cells may depend on other mechanisms rather than ANG II.
Actins ; Adult ; Angiotensin II* ; Angiotensins* ; Animals ; Atrophy ; Blotting, Western ; Dilatation ; Epithelial Cells* ; Fibroblasts* ; Fibrosis ; Humans ; Ligation ; Male ; Models, Theoretical ; Myofibroblasts ; Rats* ; Rats, Sprague-Dawley ; Ureter* ; Ureteral Obstruction* ; Vimentin

Papillary thyroid carcinoma could be a rare cause of malignant pleural effusion. The development of malignant pleural effusion in patients with papillary thyroid cancer is an extremely adverse prognostic indicator. Here, we report four cases that showed development of malignant pleural effusion during the clinical course of the papillary thyroid carcinoma and consider the prognosis. In four patients, the median survival time after the development of malignant pleural effusion was only 17 months.
Carcinoma ; Humans ; Pleural Effusion, Malignant ; Prognosis ; Thyroid Gland ; Thyroid Neoplasms

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant inherited disorder characterized by recurrent pressure palsies. Most HNPP patients have a 1.5 mb deletion in chromosome 17p11.2-p12. The present study aimed at evaluating the deletion of the 17p11.2-p12 region in Korean subjects with families exhibiting HNPP phenotype, and to determine the clinical, electrophysiological and morphological aspects specifically associated with this deletion in HNPP patients. By genotyping six microsatellite markers (D17S921, D17S955, D17S1358, D17S839, D17S122 and D17S261), HNPP with the deletion was observed in 79% (19 of 24) of HNPP families. Nerve conduction studies were performed in 35 HNPP patients from these 19 families. The observed HNPP deletion frequency in Koreans is consistent with findings in other populations. Disease onset occurred at a significantly earlier age in patients with recurrent pressure palsies than in those with a single attack (P<0.01). Nerve conduction studies demonstrated diffuse mild to moderate slowing of nerve conduction velocities that were worse over the common entrapment sites, regardless of the clinical manifestations. A long duration of compound muscle action potentials without a conduction block or a temporal dispersion is a characteristic of this disease. A sural nerve biopsy with teasing was performed in four patients, and tomacula of the myelin sheath was found in 56.4%. Our findings appear to support the existence of a phenotype/genotype correlation in HNPP patients of Korean ancestry with the deletion, and suggest that HNPP patients with earlier symptom onset face an increased chance of having recurrent attacks.
Adolescent ; Adult ; Age of Onset ; Aged ; Charcot-Marie-Tooth Disease/genetics ; Child ; Child, Preschool ; *Chromosome Deletion ; *Chromosomes, Human, Pair 17 ; DNA Mutational Analysis ; Electrophysiology ; Female ; Genotype ; Hereditary Motor and Sensory Neuropathies/*genetics/pathology/physiopathology ; Humans ; Korea ; Male ; Microsatellite Repeats ; Middle Aged ; Paralysis/*genetics/pathology/physiopathology ; Pedigree ; Phenotype ; Research Support, Non-U.S. Gov't ; Sural Nerve/pathology/physiopathology

BACKGROUND/AIMS: There have been controversial reports linking Helicobacter pylori infection to autoimmune thyroid disease (AITD). However, data regarding the relationship are limited for Asian populations, which have an extremely high prevalence of H. pylori infection. We performed this study to investigate the association between H. pylori infection and AITD in Koreans. METHODS: This study involved adults aged 30 to 70 years who had visited a health promotion center. A total of 5,502 subjects were analysed. Thyroid status was assessed by free thyroxine, thyroid stimulating hormone, and anti-thyroid peroxidase antibody (TPO-Ab). Immunoglobulin G (IgG) antibodies to H. pylori were measured as an indication of H. pylori infection. We compared the prevalence of TPO-Ab in subjects with and without H. pylori infection. RESULTS: H. pylori IgG antibodies were found in 2,875 subjects (52.3%), and TPO-Ab were found in 430 (7.8%). Individuals positive for H. pylori Ab were older than those negative for H. pylori Ab (p < 0.01). The proportion of females was significantly higher in the TPO-Ab positive group (41.0% vs. 64.2%, p < 0.01). Prevalence of TPO-Ab positivity was higher in subjects with H. pylori infection (8.6% vs. 7.00%, p = 0.03), and this association was significant after adjusting for age, sex, and body mass index (odds ratio, 1.02; 95% confidence interval, 1.00 to 1.03; p = 0.04). CONCLUSIONS: In our study, prevalence of TPO-Ab positivity is more frequent in subjects with H. pylori infection. Our findings suggest H. pylori infection may play a role in the development of autoimmune thyroiditis.
Adult ; Antibodies ; Asian Continental Ancestry Group ; Autoimmunity* ; Body Mass Index ; Cross-Sectional Studies ; Female ; Health Promotion ; Helicobacter pylori* ; Helicobacter* ; Humans ; Immunoglobulin G ; Peroxidase ; Prevalence ; Thyroid Diseases ; Thyroid Gland* ; Thyroiditis, Autoimmune ; Thyrotropin ; Thyroxine