No abstract available.
Emphysema* ; Heart Septal Defects, Ventricular*

This study was performed to investigate clinical and histopathologic features of steroid acne, which was induced by systemic administration and topical application of corticosteroids. Thirty five cases of steroid acne visited to Department of Dermatology, Hangang Sacred Heart Hospital from September, 1g79 to June, 1984 were analyzed, and the results obtained can be summarized as follows: 1. The peak age of the subjects was third decade(42.9%) with an average age of 30. 1 years, and male to female ratio was l.9: 1,2. The skin lesions had unique clinical features that showed many, uniform sized, erythematous papules and pust;ules. 3 The predilection sites of steroid acne induced by systemic steroid therapy were anterior chest(93.1%), back(44,8%), neck(31.0%), shoulder(31.0%) and face (20.7%) 4 Among thirty five cases of steroid acne, twenty cases were induced by parenteral adrninistration of dexamethasone disodium phosphate(group A), nine cases by oral administration of prednisolone(group B), and six cases by topical application of three kinds of steroid creams(group C). 5. The mean induction time after starting steroid in group A(ll. 3 days) was shorter than those in group B and C(18.9 days and l4.8 days respective)y). The mean total dosage of used steroid in group A was 191. 3mg of dexamethasone disodium phosphate and that in group B was 515. 7mg of prednisolone. On histopathologic findings of twenty two skin biopsy specimens of the three groups, perivascular inflammatory reaction was the most common finding followed by intra-and peri-follicular inflammatory reaction, dermal vascular dilatation, necrosis of follicular epithelium, comedo, intraand periollicular abscess and rupture of follicle.
Abscess ; Acne Vulgaris* ; Administration, Oral ; Adrenal Cortex Hormones ; Biopsy ; Dermatology ; Dexamethasone ; Dilatation ; Epithelium ; Female ; Heart ; Humans ; Male ; Necrosis ; Prednisolone ; Rupture ; Skin

Reconstruction of the auricle is one of the most fastidious fields in plastic and reconstructive facial surgery, because the ear is made up of complex cartilage framework arid its thin skin envelope. Insertion of carved rib cartilage is the most popular method for framework fabrication. But it has some disadvantages such as donor site morbidity, lesser flexibility of rib cartilage, difficulty in carving structure and distortion of cartilage after calving. Furthermore surgeon's talent and sufficient practice are necessary for a satisfactory result. So we introduced the concept of perichondral graft to improve the framework fabrication. In 1972 Skoog and associates reported that free perichondral grafts could be used to produce new cartilage. And several other reports supported the chondrogenesis of free perichondral graft. We molded the human ear using silicone rubbed impression material. And the eat mold was wrapped up in perichodrium of rabbit ear and placed in a subcutaneous pocket in formes of graft and flap. Six and eight weeks later, rabbits were sacrified and the newly formed cartilage framework was harvested. Grossly it showed the same appearance as the human eat and elastic property of normal cartilage. In histologic examination, it showed mature structure of normal cartilage; large lacunae containing spherical chondrocytes surrounded by well defined capsule.
Aptitude ; Cartilage ; Chondrocytes ; Chondrogenesis ; Ear ; Ear Cartilage* ; Fungi ; Humans ; Plastics ; Pliability ; Rabbits ; Ribs ; Silicones ; Skin ; Tissue Donors ; Transplants*

No abstract available.
Female ; Mammaplasty*

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

OBJECTIVE: To evaluate the usefulness of cutaneous silent period(CSP) in assessing the pain sensory function mediated by the Adelta fiber in diabetic polyneuropathy and to define the proper CSP parameter and method. METHOD: We studied 18 diabetic polyneuropathy patients and 20 age-matched healthy subjects. CSPs were recorded in the abductor pollicis brevis muscle and soleus muscle with the surface electrodes and a painful electrical stimulation was given to the mixed nerves(median and tibial nerve) and cutaneous nerve(ulnar and superficial peroneal nerve). Onset latency, end point and duration of CSP were compared between two groups. CSP parameters correlated with the motor and sensory nerve conduction parameters in diabetic polyneuropathy patients. RESULTS: CSP onset latency and end point were significantly delayed in diabetic polyneuropathy patients for both mixed nerve and cutaneous nerve stimulations. There was no difference in CSP duration between two groups. CSP onset latency was shortend and duration was prolonged in mixed nerve stimulation due to an antidromic collision, which showed a cutaneous nerve stimulation as the propor method. There was no correlation between the CSP parameters and motor and sensory nerve conduction parameters. In 3 cases, the CSPs were unable to the evoked despite the sensory nerve action potential was normally evoked. This suggests that the CSP would give an information about the Adelta fiber function than the large myelinated fiber. CONCLUSION: This study indicates that the CSP is a useful supportive electrophysiologic study to assess the Adelta fiber function in diabetic polyneuropathy. The CSP onset latency and cutaneous nerve stimulation are the useful parameter and method for the CSP.
Action Potentials ; Diabetic Neuropathies* ; Electric Stimulation ; Electrodes ; Humans ; Muscle, Skeletal ; Myelin Sheath ; Neural Conduction ; Sensation

BACKGROUND: The purpose of this study was to investigate the difference between two nailing approaches of intramedullary screw fixation, the retrograde nailing versus the anterograde nailing, on the radiological and clinical outcomes in patients with clavicle shaft fractures. METHODS: From April 2002 to August 2014, we enrolled a total of 22 patients with clavicle shaft fractures to participate in this study. Twelve patients received retrograde intramedullary nailing and 10 received anterograde nailing. The average duration of follow-up was 12 months. In all the patients, we took follow-up radiographs of the anteroposterior and the axial views to assess the postoperative radiological outcomes. We measured the visual analogue scale (VAS) score, American Shoulder and Elbow Surgeons (ASES) score, and the range of motion (ROM). RESULTS: Clinically, we did not find a statistically significant difference in the retrograde group and the anterograde group in terms of the duration to bone union, the VAS score the ASES score and the ROMs. Radiologically, we found that the difference in the clavicle shortening of the affected arm and the unaffected arm did not show a statistically significant difference at the immediate postoperative assessment. we found that the difference in the clavicle shortening of the affected arm between the immediate postoperative and the final follow-up value did not show a statistically significant difference. CONCLUSIONS: We found that both the retrograde nailing and the anterograde nailing gave a favorable outcome for clavicle shaft fractures. Although we saw evidence of clavicle shortening after intramedullary screw fixation, this was not a factor that influenced clinical outcome.
Arm ; Clavicle* ; Elbow ; Follow-Up Studies ; Fracture Fixation, Intramedullary ; Humans ; Range of Motion, Articular ; Shoulder

BACKGROUND: CTLA4 (CD152), which is expressed on the surface of T cells following activation, has a much higher affinity for B7 molecules comparing to CD28, and is a negative regulator of T cell activation. In contrast to stimulating and agonistic capabilities of monoclonal antibodies specific to CTLA-4, CTLA4Ig fusion protein appears to act as CD28 antagonist and inhibits in vitro and in vivo T cell priming in variety of immunological conditions. We've set out to confirm whether inhibition of the CD28-B7 costimulatory response using a soluble form of human CTLA4Ig fusion protein would lead to persistent inhibition of alloreactive T cell activation. METHODS: We have used CHO-dhfr cell-line to produce CTLA4Ig fusion protein. After serum free culture of transfected cell line we purified this recombinant molecule by using protein A column. To confirm characterization of fusion protein, we carried out a series of Western blot, SDS-PAGE and silver staining analyses. We have also investigated the efficacy of CTLA4Ig in vitro such as mixed lymphocyte reaction (MLR) & cytotoxic T lymphocyte (CTL) response and in vivo such as experimental autoimmune encephalomyelitis (EAE), graft versus host disease (GVHD) and skin-graft whether this fusion protein could inhibit alloreactive T cell activation and lead to immunosuppression of activated T cell. RESULTS: In vitro assay, CTLA4Ig fusion protein inhibited immune response in T cell-specific manner: 1) Human CTLA4Ig inhibited allogeneic stimulation in murine MLR; 2) CTLA4Ig prevented the specific killing activity of CTL. In vivo assay, human CTLA4Ig revealed the capacities to induce alloantigen-specific hyporesponsiveness in mouse model: 1) GVHD was efficiently blocked by dose-dependent manner; 2) Clinical score of EAE was significantly decreased compared to nomal control; 3) The time of skin-graft rejection was not different between CTLA4Ig treated and control group. CONCLUSION: Human CTLA4Ig suppress the T cell-mediated immune response and efficiently inhibit the EAE, GVHD in mouse model. The mechanism of T cell suppression by human CTLA4Ig fusion protein may be originated from the suppression of activity of cytotoxic T cell. Human CTLA4Ig could not suppress the rejection in mouse skin-graft, this finding suggests that other mechanism except the suppression of cytotoxic T cell may exist on the suppression of graft rejection.
Animals ; Antibodies, Monoclonal ; B7 Antigens ; Blotting, Western ; Cell Line ; Electrophoresis, Polyacrylamide Gel ; Encephalomyelitis, Autoimmune, Experimental ; Graft Rejection ; Graft vs Host Disease ; Homicide ; Humans ; Immunosuppression ; Lymphocyte Culture Test, Mixed ; Lymphocytes ; Mice ; Silver Staining ; Staphylococcal Protein A ; T-Lymphocytes

No abstract available.