No abstract available.
Antibodies, Monoclonal* ; Treponema pallidum* ; Treponema*

No abstract available.
Hepatitis B* ; Hepatitis*

No abstract available.
Acyclovir* ; Necrosis*

PURPOSE: Recently developed BMS(TM) (Zassi Bowel Management System(TM): Hollister Inc., Illinois, USA) can provide effective nonsurgical fecal diversion without the risks associated with colostomy creation and subsequent closure. Our aim is to evaluate the effectiveness of the BMS in diverting feces from the perianal wide surgical wound in patients with Fournier's gangrene. METHODS: BMS(TM) was applied in five patients (male: 2, median age; 44) with Fournier's gangrene from January 2000 to September 2001. The treatments consist of three times a day wound dressing after wide surgical debridement and intravenous antibiotic therapy. For evacuation of feces, twice daily warm saline irrigation was administered via BMS(TM) or low daily doses of polyethylene glycol solutions were orally taken in. An endoscopic and anorectal manometric study was done to evaluate possible mucosal complications and anorectal functional changes. RESULTS: The average duration of the BMS application was 41 (range, 22~63) days. The result of a manometric study after immediate removal of the BMS(TM) showed a decreased mean resting pressure (range: 22~36 mmHg) and a decreased mean squeezing pressure (range: 32~39 mmHg). After 3 days, the sphincter pressure had improved markedly: mean resting pressures of 38, 45, 60, and 63 mmHg and mean squeezing pressure of 78, 89, 91, and 101 mmHg respectively. Fecal incontience was not noted in any patient. Other possible mucosal complications were not noted. There were no mortalit. CONCLUSIONS: BMS(TM) application in Fournier's gangrene patients after surgery successfully avoids a defunctioning colostomy. Furthermore, no significant complications were noted over a prolonged period up to 63 days.
Bandages ; Colostomy ; Debridement ; Fasciitis, Necrotizing ; Feces ; Fournier Gangrene ; Humans ; Illinois ; Polyethylene Glycols

Deep skin and soft tissue defects with exposed bone and tendon is difficult to treat, because skin graft rarely survives and flap surgery is sacrifice of donor site. Since "Stage I" membrane was developed by Yannas and Bruke in 1980, numerous kinds of artificial skin have been developed. The adaptability of "Terudermis", developed by the Terumo Co., as an artificial skin composed of sponge made of a fibrillar atelocollagen and a heat-denatured atelocollagen, was clinically evaluated on application to 13 cases presenting deep skin and soft tissue defect with exposed bones and tendons from October 1997 to march 1998. Terudermis has the advantage of allowing early incorporation of fibroblasts and capillaries into its collagen sponge due to very weak dehydrothermal cross-linking. Before Terudermis graft, several days of wet dressing and debridement were required to prepare healthy well-vascularized bed because Terudermis was weak on unsanitary wounds. After bed preparation, Terudermis was grafted like usual skin graft. Tie-over bolster dressing or compressive dressing was used case by case. The dressing was opened 2~3 days after Terudermis grafting. Wet dressing was done daily until the skin graft was done. Autologous skin graft was done 2-3 weeks after Terudermis graft. Our clinical results indicated that Terudermis was beneficial in treating 77% of our patients. Through the use of this new method, treatment of severe skin and soft tissue defects that are usually treated by musculocutaneous or other conventional skin flaps can be replaced by Terudermis as an new artificial dermis.
Bandages ; Capillaries ; Collagen ; Debridement ; Dermis ; Fibroblasts ; Humans ; Membranes ; Porifera ; Skin ; Skin, Artificial ; Tendons ; Tissue Donors ; Transplants ; Wounds and Injuries*

We built the hypothesis that the hypertrophic callus formation is mediated by beta-endorphin that stimulates secretion of GH and increase circulation growth factor activity in head injury patient. We classified 4 groups such as 5 normal person(control), group I;5 patients with only fracture, group II;5 patients with fracture and head injury, group III; 5 patients with only head injury, group IV. We obtained the samples of serum from each group at 0, 2, 4, 6, 8 weeks after trauma and assessed the serum level of GH, GHRH, somatostatin. The serum level of GH was statisticallyu higher in group III, IV than group I, II. There was not significant difference in serum level of GHRH. The serum level of somatostatin was higher in group II, III, IV than group I, but there was no statistical significance in each group. GH has a important role in hypertrophic callus formation in severe head injury patients, but there was no evidence that the mechanism is mediated by beta-EndorphinGHRH & somatostatin-GH-GF-1, beta-FGF axis. There may be a another mechanism in increasing GH that was stimulated by beta-endorphin in thalamus and lateral ventricle, and it should be necessary for further evaluation of it.
Axis, Cervical Vertebra ; beta-Endorphin ; Bony Callus ; Craniocerebral Trauma* ; Head* ; Humans ; Lateral Ventricles ; Somatostatin ; Thalamus

In order to investigate causative mechanisms of optic neuropathy, retrospective clinical studies including ophthalmologic examination, imaging study, and molecular biologic analyses were performed on 322 patients with optic neuropathy. The causes include hereditary optic neuropathy(71 patients, 22.1%), optic neuritis(66 patients, 20.5%), traumatic optic neuropathy(40 patients, 12.5%), ischemic optic neuropathy(35 patients, 10.9%), compressive optic neuropathy(31 patients, 9.6%), toxic optic neuropathy(23 patients, 7.1%), etc. In 29 patients of bilateral optic atrophy and 18 patients of unilateral optic atrophy, the causative mechanism was not clear. In conclusion, hereditary optic neuropathy was the most common causative mechanism of optic neuropathy in this study. The importance of meticulous history taking and molecular biologic test should be stressed in differential diagnosis of optic neuropathy.
Diagnosis, Differential ; Humans ; Optic Atrophy ; Optic Nerve Diseases* ; Optic Nerve Injuries ; Optic Neuritis ; Retrospective Studies

In order to investigate causative mechanisms of optic neuropathy, retrospective clinical studies including ophthalmologic examination, imaging study, and molecular biologic analyses were performed on 322 patients with optic neuropathy. The causes include hereditary optic neuropathy(71 patients, 22.1%), optic neuritis(66 patients, 20.5%), traumatic optic neuropathy(40 patients, 12.5%), ischemic optic neuropathy(35 patients, 10.9%), compressive optic neuropathy(31 patients, 9.6%), toxic optic neuropathy(23 patients, 7.1%), etc. In 29 patients of bilateral optic atrophy and 18 patients of unilateral optic atrophy, the causative mechanism was not clear. In conclusion, hereditary optic neuropathy was the most common causative mechanism of optic neuropathy in this study. The importance of meticulous history taking and molecular biologic test should be stressed in differential diagnosis of optic neuropathy.
Diagnosis, Differential ; Humans ; Optic Atrophy ; Optic Nerve Diseases* ; Optic Nerve Injuries ; Optic Neuritis ; Retrospective Studies

Purpose : Shortness is the most frequent and quite disturbing characteristics of patients with Turner syndrome. The aim of this study was to evaluate the factors affecting final adult height(FAH) in these patients. METHODS : The study group was comprised of 19 patients who were diagnosed as Turner syndrome and attained FAH. We analyzed the influences of various factors on FAH in GH treated group with those in GH untreated group. Results : Nineteen patients were enrolled; thirteen received GH treatment and six did not. The mean duration of GH treatment was 24.3 months(range : 9 to 50 months), and the mean dosage of GH was 0.98+/-0.35IU/kg/wk in GH treated group. The mean growth velocity during GH treatment was 5.6+/-1.8 cm/yr, which was significantly higher than that during pretreatment period(P<0.05). In GH treated group, the mean chronological age, bone age, mean height, and height SD score at GH therapy were 13.7+/-1.7yr, 11.3+/-1.9yr, 129.7+/-7.9cm, and -4.1+/-1.1, respectively, which were not statistically different from those at diagnosis of GH untreated group. In GH treated group, the mean FAH and FAH SD score were 144.8+/-5.0cm, and -3.2+/-0.9, respectively, which showed no significant difference compared with those of GH untreated group. Analyzing the factor affecting FAH in all Turner girls of both groups together, parental height, chronological age, bone age, and bone age delay at diagnosis(or at the initiation of GH therapy) were not related to FAH. Height and height SD score at diagnosis(or at the initiation of therapy) were positively related to FAH(P<0.05, r=0.72). CONCLUSION : The results suggest that GH treatment dose not improve FAH in patients with Turner syndrome, despite increased growth velocity during GH treatment, which might come from intermittern GH therapy. This should be remained to be clarified with more Turner patients who attained FAH.
Adult* ; Diagnosis ; Female ; Growth Hormone ; Humans ; Parents ; Turner Syndrome*

The presence and distribution of pan-neuroendocrine markers such as neuron-specific enolase (NSE), chromogranin (CG), and synaptophysin (SYP) were investigated by immunohistochemistry in 15 cases of neuroblastic tumors, including four cases of neuroblastomas, six cases of ganglioneuroblastomas, and five cases of ganglioneuromas. Three cases of normal sympathetic ganglion were used for the normal control group. NSE was observed in all cases and both in ganglion cells and in neuropils. NSE was detected not only in the majority of the neuroblasts showing signs of differentiation, but also in some poorly differentiated neuroblasts. All cases of neuroblastic tumors were positive for CG, however, some variability of staining intensity and distribution patterns were noted. CG was found mainly in differentiated neuroblasts with enlarged cytoplasm and nuclei along the periphery of the perikaria, and was also found in the perinuclear regions of some undifferentiated cells. SYP was positive in 9 of 11 cases. In all of the 9 cases, SYP was detected in some differentiating neuroblasts and differentiated neuroblasts, as well as the mature ganglion cells. However, it has scarcely stained in dot or granular pattern. Two CG-negative tumors were also negative for SYP. Our data indicate that antibodies against NSE and CG are helpful as a diagnostic aid for neuroblastic tumors.
Antibodies ; Cytoplasm ; Ganglia, Sympathetic ; Ganglion Cysts ; Ganglioneuroblastoma ; Ganglioneuroma ; Immunohistochemistry ; Neuroblastoma ; Neurons* ; Neuropil ; Phosphopyruvate Hydratase* ; Synaptophysin*