Twenty to twenty-five percent of patients are reported to experience problems with anorectal function after low anterior resection, complaining particularly urgency of defecation and minor fecal leakage, but the mechanisms underlying its cause and the recovery process are not well understood. We designed this study to elucidate the mechanism of anorectal functional problems and its recovery process after low anterior resection for rectal cancer by autonomic nerve preserving procedure. Standardized interviews and anorectal physiologic studies including balloon proctometry and manometry were performed in 32 patients preoperatively, and at 1 month, 3 months, 6 months and 1 year after the operation. Postoperatively stool frequency increased, the ability to defer defecation and discriminate stool characters were compromised, and anal incontinence scores increased, which recovered progressively by 6~12 months after the operation. Balloon proctometry showed that threshold volume, urgent volume and maximal tolerable volume decreased remarkably after the operation. The latter two parameters recovered considerably by 1 year after the operation. Rectal compliance also decreased significantly but it showed no evidence of recovery by 1 year after the operation. Anorectal manometry showed that maximum anal resting pressure decreased significantly after the operation which recovered significantly by 1 year after the operation. Maximum anal squeeze pressure showed no significant decrease after the operation. In most patients rectoanal inhibitory reflex was abolished after the operation, which recovered only in some cases by after 1 year. The group of short residual rectum(<4 cm, N=18) showed more impairment in continence and decrease in neorectal capacity and compliance than that of the long residual rectum(> or =4 cm, N=14). These results suggest impairment in fecal continence occurs due to decrease in rectal capacity, compliance, and anal canal pressure, and loss of rectoanal inhibitory reflex. Autonomic nerve preserving procedure could not prevent the decrease in resting anal pressure. Continence recovers clinically with increase in neorectal capacity, compliance and anal canal pressure but not with recovery of rectoanal inhibitory reflex. The length of the residual rectum seems to play an important role in the degree of impairment of continence and good continence can be expected when the residual rectum is more than 4 cm.
Anal Canal ; Autonomic Pathways ; Compliance ; Defecation ; Humans ; Manometry ; Rectal Neoplasms ; Rectum ; Reflex

PURPOSE: When Managing metastatic bladder tumors, to overcome the resistance mechanism of cisplatin is a main problem to be solved. The objective is to confirm the changes of general and ultrastructural morph ology with the induction of cisplatin resistance from the bladder cell line. MATERIALS AND METHODS: The samples of this investigation are 2ng/ml-cisplatin resistant human bladder cell lines T24R2 established by SNUH Urology and the drug resistant bladder cell lines T24 was obtained from ATCC, as a control group. We cultured the resistant cell line on the slide and observed it using light microscopy to see the general morphology. For the ultrastructural morphology, we fixed cultured cells, made an epon block, sliced an ultrathin section and observed it using H-71000 EM. RESULTS: Under light microscopy, the cytoplasm of the resistant cell line shows a plumper pattern than that of the parent cell. Under electronmicroscopy, the chromatin of the resistant cell line has a relatively finely dispersed chromatin pattern when compared to the parent cell line, which shows a coarse and aggregated chromatin pattern. Within the cytoplasm, the mitochondrial volume, dilated rough endoplasmic reticulum, polyribosomes and ribosomes are moderately increased in the resistant cell line when compared to the parent cell line. In particular, we found a great amount of double membrane vesicle near the cell surface and pinocytic vesicles on the surface, which are seldom observed within the parent cells. CONCLUSIONS: We concluded that the cisplatin resistant human bladder cell lines (T24R2) underwent a morphological change with the induction of cisplatin resistance, and we hypothesize that the resistant cell's ultrastructure, which shows morphological change, will be involved in the drug resistance mechanism. Regarding this matter, further research will be needed.
Cell Line* ; Cells, Cultured ; Chromatin ; Cisplatin* ; Cytoplasm ; Drug Resistance ; Endoplasmic Reticulum, Rough ; Humans ; Membranes ; Microscopy ; Mitochondrial Size ; Parents ; Polyribosomes ; Ribosomes ; Urinary Bladder Neoplasms ; Urinary Bladder* ; Urology

No abstract available.
Humans ; Mucocele*

No Abstract Available.
Anisometropia*

No abstract available.
Arnold-Chiari Malformation* ; Diagnosis* ; Prenatal Diagnosis* ; Ultrasonography*

No abstract available.
Compliance* ; Oxygen* ; Positive-Pressure Respiration* ; Respiratory Insufficiency* ; Ventilation*

No abstract available.
Compliance* ; Oxygen* ; Positive-Pressure Respiration* ; Respiratory Insufficiency* ; Ventilation*

Diastematomyelia is an uncommon congenital malformation of the vertebral axis characterized by a localized longitudinal separation of the spinal cord with an interposed septum. It may be found in association with congenital scoliosis. The Authors experienced a case of congenital scoliosis with diastematomyelia. Diastematomyelia was surgicallv resected and scoliosis was corrected by Dwyer operation 5 months later. The results of both operations were satisfactory in 10 months follow up.
Follow-Up Studies ; Neural Tube Defects ; Scoliosis ; Spinal Cord

No abstract available.
Hypnotics and Sedatives*

BACKGROUND: Since the exact pathogenesis of sepsis-induced ARDS has not been elucidated, the mechanisms of enhanced neutrophilic respiratory burst were probed in endotoxin primed neutrophils associated with the roles of phospholipase A2 (PLA2), platelet activating factor (PAF) and apoptosis. METHODS: In isolated fresh human neutrophils, effects of the inhibition of PLA2 and PAF on the apoptosis were examined by the method of Annexin-FITC/dual PI flow cytometry. The roles of PLA2 and PAF on the neutrophilic respiratory burst were also examined by measuring oxidant generation in cytochrome-c reduction assay. Activities of the PLA2 and lysoPAF acetyltransferase (lysoPAF AT) of the neutrophils were determined to understand the effect of endotoxin on these enzymatic activities which may be related to the neutrophilic respiratory burst and apoptosis. In addition, the role roles of PLA2 and PAF in neutrophilic adhesion to bovine endothelial cells were examined in vitro by neutrophil adhesion assay. To investigate the effect of oxidants on pulmonary surfactant, cytochemical ultrastructural microscopy was performed. To inhibit PLA2 and PAF, non-specific PLA2 inhibitor mepacrine (100 nM) and WEB 2086 (100 nM) or ketotifen fumarate (10 kg/ml) were used respectively in all in vitro experimental sets. WEB 2086 is PAF receptor antagonist, and ketotifen fumarate is a lyso PAF AT inhibitor. RESULTS: The mapacrine treatment, provided after the endotoxin (ETX) treatment, resulted in increased apoptosis of neutrophils (p<0.001) while treatments of WEB 2086 and ketotifen did not. The inhibition of PLA2 and PAF decreased (p<0.001) production of oxidants from PMA-stimulated neutrophils. While endotoxin increased the PLA2 activity of neutrophils (p<0.01), mepacrine supressed (p<0.001) the activity, provided after treatment of ETX. The lyso PAF actyltransferase activity (lyso PAF AT) increased(p<0.01) after treatment of ETX. In contrast, mepacrine, WEB 2086 and ketotifen showed a tendency of decreasing the activity after treatment of ETX. The Treatment of ETX increased (p<0.001) neutrophil adhesion to endothelial cells, which was reversed by inhibition of PLA2 and PAF (p<0.001). The binding of oxidants to pulmonary surfactant was identified histologically. CONCLUSIONS: The enhanced neutrophilic respiratory burst by ETX plays a pivotal role in the pathogenesis of ARDS in term of oxidayive oxidative stress. Increased production of oxidants form neutrophils is mediated by the activations of PLA2 and lyso PAF AT.
Apoptosis* ; Endothelial Cells ; Flow Cytometry ; Humans ; Ketotifen ; Microscopy ; Neutrophils* ; Oxidants ; Oxidative Stress ; Phospholipases A2 ; Platelet Activating Factor ; Pulmonary Surfactants ; Quinacrine ; Respiratory Burst*