The isoimmune hemolytic disease of newborn due to the minor blood groups is characterized by the progressive neonatal hyperbilirubinemia and anemia. This is caused by the lgG antibody transmitted from the mother to the fetus across the placenta. ABO and Rho(D) incompatability have been the most common antibody responsible for hemolytic disease of newborn. But recently the incidence of the Rho(D) incompatability is decreased due to the prophylaxis of anti-D immunoglobulin for the Rh negative mother and that of the incompataibility of minor blood group seems to be increased. This report presents the clinical and hematologic features of four cases of hemolytic diseases of newborn due to minor blood group isoimmunization who were admitted to the Dong-guk University Kyung-ju Hospital. The following results were obtained; 1) Neontal hyperbilirubinemia was observed within 48 hours after birth in all cases of patients and disappeared with the treatment of exchange transfusion and phototherapy. 2) Total bilirubin levels were 6.7-24.8 mg/dl. 3) Direct Coombs' test was positive in all cases of patients and indirect Coombs' test was positive except case 3. Direct Coombs' test was negative and indirect Coombs' test was positive in all mothers. 4) There was no evidence of ABO or Rh(D) incompatibility in all cases of patients. Case 1, 2 and 4 had the hemolytic diseases of newborn due to anti-E isoimmunization anti-E, but case 3 had the hemolytic diseases of newborn due to anti-C isoimmunization. 5) According to the reports which was published to date, 23 cases of the hemolytic diseases of newborn due to minor blood group isoimmunization were revealed; 14 anti-E, 4 anti-c, 1 anthE or c, 1 anti-C, 1 anti-e, 1 anti-M, and 1 anti-Kidd. Therefore we can easily conclude that anti-E is the most common cause of hemolytic diseases of newborn due to minor blood group isoimmunization in Korea. So, we report this case with the brief review of relevant literatures.
Anemia ; Bilirubin ; Blood Group Antigens ; Coombs Test ; Erythroblastosis, Fetal ; Fetus ; Gyeongsangbuk-do ; Humans ; Hyperbilirubinemia ; Hyperbilirubinemia, Neonatal ; Immunoglobulins ; Incidence ; Infant, Newborn ; Korea ; Mothers ; Parturition ; Phototherapy ; Placenta

No abstract available.
Erythroblastosis, Fetal* ; Humans ; Infant, Newborn ; Siblings*

No abstract available.

Bakground : Patient-Controlled Analgesia (PCA) has become popularized for postoperative pain control. Theoretically, addition of a basal infusion would ameliorate the pain control as related to less need for additional demands. Regardless of theoretical background, usefulness of a basal infusion in PCA is controversial. Therefore, in this study we compared the analgesic consumption between PCA only and PCA plus basal infusion and assessed if the use of a basal infusion improves the analgesic efficacy in intravenous PCA. METHODS: 40 patients undergoing caesarian section, were assigned randomly to PCA only group (group 1) and PCA plus basal infusion group (group 2). Group 1 was programmed to deliver 1.5 ml of bolus infusion with 10 minutes of lockout interval and four times per hour of the maximum usage of patient control module. In group 2, 0.5 ml of basal infusion was added to the same PCA. The analgesic solution contained 60 mg of morphine, 180 mg of ketorolac and 5 mg of droperidol in total volume of 60 ml. PCA was started at the time of the peritoneal closure with 2 ml of loading dose in all patients. Postoperative assessments were pain score, sedation score, side effect, total analgesic consumption and the degree of patients, satisfaction. RESULTS: Total analgesic consumption was significantly greater in group 2 than in group 1. Pain score, sedation score, complication and the degree of the satisfaction were almost the same at all time interval in each group. CONCLUSION: We concluded that there was no significant benefit of basal infusion in intravenous PCA after caesarean section.
Analgesia ; Analgesia, Patient-Controlled* ; Cesarean Section* ; Droperidol ; Female ; Humans ; Ketorolac ; Morphine ; Pain, Postoperative ; Passive Cutaneous Anaphylaxis ; Pregnancy

No abstract available.
Adult* ; Female* ; Humans

Treatments of tibia shaft fracture are closed reduction followed by cast immobilization, external fixation, intramedullary nailing and internal fixation with plate and screws. Among these, intramedullary nailing is commonly used method today. The tibia nailing has high rate of union, but malunion, infection, the joint stiffness and anterior knee pain develops frequently. We reviewed the clinical and radiological result of anterior knee pain retrospectively after tibia nailing. The result were as follows: l. Age distribution of tibia shaft fracture was 17 to 76, and mean age was 40 male patients were 35 and female 13. 2. The open fractures were 17 and the closed fractures were 34. 3. The causes of' tibia shaft fracture were traffic accidents(30cases), fall down injuries(6 cases), slip down injuries(1 1 cases) and other injuries(4 cases) Among the these, 19 cases were cornbined with other fractures or neuri.isurgical injuries. 4. The incision methods were recorded as follows: parapatella tendon incision were 9 cases, patella splitting incision were 25 cases and unrecorded were 17cases. 5. According to the radiological analysis, the average nail plateau distance was 10.3mm and the extent of nail protrusion beyond the anterior cortex was -1.73mm. Among these, protrusion of proximal targeting screws were 8 cases. 6. Insertion of nail through the patella tendon was associated with a hipher incidence of knee pain compared to paratendon site of insertion. The extent of nail protrusion were related to anterior knee pain after tibia intramedullary nailing.
Age Distribution ; Female ; Fracture Fixation, Intramedullary* ; Fractures, Closed ; Fractures, Open ; Humans ; Immobilization ; Incidence ; Joints ; Knee* ; Male ; Patella ; Patellar Ligament ; Retrospective Studies ; Tendons ; Tibia*

No abstract available.
Crohn Disease*

BACKGROUND: We previously demonstrated that a GRE/TRE composite sequence, which is located between 200 bp and 220 bp relative to the transcriptional start site of rat TRH gene, is responsible for the dexamethasone (DEX)- and TPA-induced transcriptional activation, and the transcriptional activation by DEX is mediated by interaction between glucocorticoid receptor (GR) and a TRE-binding transcriptional factor such as c-Jun. However, a non-specific binding with the transciption factors can not be excluded as the mutants used in the previous report could not inhibit the binding of GR and c-Jun completely, and it remains unclear which one of the two TRE-like sequences is critical for the interaction of the two transcription factors. METHODS: Luciferase expressing plasmids that contain a part of rat TRH promoter including the composite GRE sequence or its mutants were transfected into HeLa cells by Fugene 6. After the cells were incubated overnight with DEX or/and TPA, the luciferase activity was measured in a chemiluminometer. A gel retardation assay was performed after binding of the labeled composite sequence or its mutants with GR and c-Jun. RESULTS: DEX and TPA increased the transcriptional activity of the wild type composite sequence by 3 folds and 4 folds, respectively, and the combined stimulation increased the activity by 10 folds. The mutants of which all 6 nucleotides of the GRE half site were replaced and removed almost did not bind to GR and eould not enhance the transcriptional activity at all in response to DEX. The GRE-deleted mutant bound to c-Jun with a remarkably lower affinity and showed a lower response to TPA, whereas the GRE-replaced mutant bound to c-Jun with a similar affinity and showed a similar response to TPA compared to those of the wild type. In response to the combined simulation with DEX and TPA, the mutants showed 30-40% of the trancriptional activity of the wild type. Basal transcriptional activity of all the TRE mutants was significantly lower than that of the wild type. While they almost could not bind to c-Jun, their binding affinity to GR was comparable to that of the wild type. Whereas the DEX- and TPA-induced transcriptional activity of 5 TRE mutant was 10% and 15% of that of the wild type, it responded to those agents in a similar pattern as the wild type. The 3 TRE mutant and the mutant of both TRE sites did not respond to DEX and TPA. The GRE-deleted mutant hardly formed the DNA-protein complex as did the wild type, while the GRE -replaced mutant could form the complex in a less amount with nuclear extract of HeLa celL CONCLUSION: These results suggest that GRE/TRE composite sequence of rat TRH gene specifically binds to GR and c-Jun, providing a site for interaction between the two transcription factors, and that both TRE sites play an important role in basal transcription, and that the 3 TRE site is more critical in the interaction between GRE and TRE for DEX-induced transcriptional activation. (J Kor Endocrinol 14:278-292, 1999)
Animals ; Dexamethasone ; Electrophoretic Mobility Shift Assay ; HeLa Cells ; Humans ; Luciferases ; Mutagenesis, Site-Directed* ; Nucleotides ; Plasmids ; Rats* ; Receptors, Glucocorticoid ; Response Elements* ; Transcription Factors ; Transcriptional Activation

BACKGROUND: We previously demonstrated that the promoter of rat TRH gene has GRE half site (TGTTCT) between -210 bp and -205 bp flanking with similar sequences of TPA response element (TRE), TAGTCA, at a distance of several base pairs from the GRE half site. It promps us to hypothesize that this composite GRE/TRE sequence can provide a site for interaction between glucocorticoid receptor (GR) and c-Jun. Thus, we investigated whether the composite sequence mediates transcriptional regulation induced by dexamethasone (DEX) and 12-O-tetradecanoyl phobol-13-acetate (TPA), and whether it binds GR and c-Jun. METHODS: A luciferase expressing plasmids that contain a part of rat TRH promoter including the composite sequence or their mutants were transfected into HeLa cells by Fugene 6. After the cells were incubated overnight with DEX and TPA, the luciferase activity was measured in a chemiluminometer. A gel retardation assay was performed after binding of the labeled composite sequence or its mutants with GR and c-Jun. RESULTS: DEX increased the transcriptional activity of the plasmid containing the wild type GRE by 2.5 folds, and TPA increased the transcriptional activity by 4 folds. The simultaneous stimulation with DEX and TPA synergistically increased the transcriptional activity by 10 folds. Two mutants whose GRE half sits were altered showed no responses to DEX, and suppressed the TPA-induced or both agents-induced transcriptional activity by 50%. Two mutants whose TRE-like sites were altered suppressed the DEX-induced transcriptional activity by 20%, TPA-induced trarptional activity by 25%, and both agents-induced transcriptional activity by 50%. Gel retardation assay showed that the composite sequence fonned a complex with GR and its mutants bound to GR with remarkably less affinity. c-Jun also bound to the composite sequence to form two cornplexes with less affinity compared to the AP-1 consensus sequence. The mutants of the TRE-like sequence bound to c-Jun with a significantly lower affinity compared to that of the wild type. Simulateous binding of the composite sequence with GR and c-Jun did not form any larger complex. The complex of GR and the composite sequence was much smaller than that formed by c-Jun, suggesting that GR binds to the composite sequence as a monomer. CONCLUSION: These results suggest that the composite sequence of GRE half site and TRE-like site on the promoter of rat TRH gene provides binding sites for GR and c-Jun, which mediate the interaction between two signal transduction pathways. (J Kor Soc Endocrinol 14:265-277, 1999)
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid ; Animals ; Base Pairing ; Binding Sites ; Consensus Sequence ; Dexamethasone ; Electrophoretic Mobility Shift Assay ; HeLa Cells ; Humans ; Luciferases ; Plasmids ; Rats ; Receptors, Glucocorticoid ; Response Elements ; Signal Transduction ; Transcription Factor AP-1

No abstract available.
Leukemia* ; Skin*