No abstract available.
Down Syndrome* ; Leukemia, Megakaryoblastic, Acute*

No abstract available.

Infection in primary total hip arthroplasty may cause catastrophic results and is the major reason for implant failure. The purpose of this study was to evaluate the utility of the hip joint fluid culture as a method of predicting the possibility of a hip joint infection by calculating the sensitivity, specificity and accuracy. We performed 628 primary total hip arthroplasty and aerobic and anaerobic bacterial cultures for hip joint fluid between January 1989 and June 1996. The hip joint fluid culture was routinely performed to evaluate the utility of the femoral head for bone banking. Thirty-two cases out of the 628 hips showed positive intraoperative culture and 596 cases showed negative intraoperative culture. The isolated organisms from 32 positive cultures were 11 for Staphylococcus aureus, eight for Staphylococcus coagulase negative, seven for Enterococcus, three for E.coli and one each for Enterobacter, Acinetobacter and Pseudomonas. Anaerobic culture was negative in all cases. In the positive intraoperative culture cases, none had delayed infection during the follow-up period. But in the negative intraoperative culture cases, one case had acute infection and two cases had delayed infection. In the case with acute infection, Staphylococcus aureus was isolated and on two cases with delayed infection, Enterococcus and Staphylococcus coagulase negative were isolated, respectively. All 32 positive culture cases were fa~lse positive and 595 negative culture cases were true negative and one negative culture case was fa~lse negative. The sensitivity of the hip joint culture was 0%, the specificity was 94.9% and the accuracy was 0%. The specificity of hip joint fluid culture in primary total hip arthroplasty was high, hut the sensitivity score was zero. Therefore, the hip joint fluid culture should not be used for a routine check of infection status in primary total hip arthroplasty. We recommend the hip joint fluid culture in revision arthroplasty or hips in which infection is clinically suspected.
Acinetobacter ; Arthroplasty ; Arthroplasty, Replacement, Hip* ; Bone Banks ; Coagulase ; Enterobacter ; Enterococcus ; Follow-Up Studies ; Head ; Hip Joint* ; Hip* ; Pseudomonas ; Sensitivity and Specificity ; Staphylococcus ; Staphylococcus aureus

OBJECTIVE: The purpose of this study was to investigate the effect of using laser for ceramic bracket bonding of porcelain surfaces and to compare it with conventional treatment of porcelain surfaces. METHODS: Ninety feldspathic porcelain specimens were divided into 9 groups of 10, with each group having different surface treatments performed. Surface treatment groups were orthophosphoric acid, orthophosphoric acid with silane, hydrofluoric acid, hydrofluoric acid with silane, sandblasted, sandblasted with silane, laser etched, laser etched with silane, and glazed surface served as a control group. In the laser etched groups, the specimens were irradiated with 2-watt superpulse carbon dioxide (CO2) laser for 20 seconds. Ceramic brackets were bonded with light-cure composite resin and all specimens were stored in water at 37degrees C for 24 hours. Shear bond strength was determined in megapascals (MPa) by shear test at 1 mm/minute crosshead speed and the failure pattern was assessed. For statistical analysis, one-way ANOVA and tukey test were used. RESULTS: Statistical analysis showed significant differences between the groups. The HFA + S group showed the highest mean shear bond strength (13.92 +/- 1.94 MPa). This was followed by SB + S (10.16 +/- 1.27 MPa), HFA (10.09 +/- 1.07 MPa), L + S (8.25 +/- 1.24 MPa), L (7.86 +/- 0.96 MPa), OFS + S (7.22 +/- 1.09 MPa), SB (3.41 +/- 0.37 MPa), OFA (2.81 +/- 0.37 MPa), G (2,46 +/- 1.36 MPa). Bond failure patterns of HFA and silane groups, except L + S, were cohesive modes in porcelain while adhesive failure was observed in the control group and the rest of the groups. Conclusions : A 2-watt superpulse CO2 laser etching of porcelain surfaces can provide a satisfactory result for porcelain surface treatment for ceramic bracket bonding. Laser irradiation may be an alternative conditioning method for the treatment of porcelain surfaces.
Adhesives ; Carbon Dioxide ; Ceramics ; Dental Porcelain ; Hydrofluoric Acid ; Lasers, Gas ; Phosphoric Acids ; Water

To assess the relationship between angiotensin-converting enzyme (ACE) gene polymorphism and myocardial infarction in Koreans, we recruited 112 healthy, unrelated subjects (mean age 53.4 years) and 104 myocardial infarction survivors (mean age 54.2 years) of both sexes. An insertion/deletion (IID) polymorphism of the ACE gene was typed by polymerase chain reaction. The I allelic frequency of ACE gene in Korean subjects was irrelevant to myocardial infarction (patients, 65%; control subjects 66%), as was true with the D allele. When compared with other populations, the frequency of D allele in Koreans (0.34) was lower than that in Caucasians, and was close to that of other Oriental populations. The data suggest that the ACE gene polymorphism is not an independent genetic risk factor for myocardial infarction in Koreans.
Alleles ; Asian Continental Ancestry Group ; Humans ; Myocardial Infarction* ; Polymerase Chain Reaction ; Risk Factors ; Survivors

No abstract available.
Osteotomy ; Ultrasonics

Contraction of smooth muscle is initiated by an increase in cytosolic Ca2+ leading to activation of Ca2+/calmodulin-dependnet myosin light chain (MLC) kinase and phosphorylation of MLC. The types of contraction and signaling mechanisms mediating contraction differ depending on the region. The involvement of these different mechanisms varies depending on the source of Ca2+ and the kinetic of Ca2+ mobilization. Ca2+ mobilizing agonists stimulate different phospholipases (PLC-beta, PLD and PLA2) to generate one or more Ca2+ mobilizing messengers (IP3 and AA), and diacylglycerol (DAG), an activator of protein kinase C (PKC). The relative contributions of PLC-beta, PLA2 and PLD to generate second messengers vary greatly between cells and types of contraction. In smooth muscle cell derived form the circular muscle layer of the intestine, preferential hydrolysis of PIP2 and generation of IP3 and IP3-dependent Ca2+ release initiate the contraction. In smooth muscle cells derived from longitudinal muscle layer of the intestine, preferential hydrolysis of PC by PLA2, generation of AA and AA-mediated Ca2+ influx, cADP ribose formation and Ca2+/-induced Ca2+ release initiate the contraction. Sustained contraction, however, in both cell types is mediated by Ca2+/-independent mechanism involving activation of PKC- epsilon by DAG derived form PLD. A functional linkage between G13, RhoA, ROCK, PKC- epsilon, CPI-17 and MLC phosphorylation in sustained contraction has been implicated. Contraction of normal esophageal circular muscle (ESO) in response to acetylcholine (ACh) is linked to M2 muscarinic receptors activating at least three intracellular phospholipases, i.e. phosphatidylcholine-specific phospholipase C (PC-PLC), phospholipase D (PLD) and the high molecular weight (85 kDa) cytosolic phospholipase A2 (cPLA2) to induce phosphatidylcholine (PC) metabolism, production of diacylglycerol (DAG) and arachidonic acid (AA), resulting in activation of a protein kinase C (PKC)-dependent pathway. In contrast, lower esophageal sphincter (LES) contraction induced by maximally effective doses of ACh is mediated by muscarinic M3 receptors, linked to pertussis toxin-insensitive GTP-binding proteins of the Gq/11 type. They activate phospholipase C, which hydrolyzes phosphatidylinositol bisphosphate (PIP2), producing inositol 1, 4, 5-trisphosphate (IP3) and DAG. IP3 causes release of intracellular Ca2+ and formation of a Ca2+/-calmodulin complex, resulting in activation of myosin light chain kinase and contraction through a calmodulin-dependent pathway.
Acetylcholine ; Arachidonic Acid ; Cyclic ADP-Ribose ; Cytosol ; Esophageal Sphincter, Lower ; GTP-Binding Proteins ; Hydrolysis ; Inositol ; Intestines ; Metabolism ; Molecular Weight ; Muscle, Smooth* ; Myocytes, Smooth Muscle ; Myosin Light Chains ; Myosin-Light-Chain Kinase ; Negotiating ; Phosphatidylcholines ; Phosphatidylinositols ; Phospholipase D ; Phospholipases ; Phospholipases A2 ; Phosphorylation ; Phosphotransferases ; Protein Kinase C ; Receptor, Muscarinic M3 ; Receptors, Muscarinic ; Second Messenger Systems ; Type C Phospholipases ; Whooping Cough

Postoperative ileus (POI), a symptom that occurs after abdominal surgery, reduces gastrointestinal motility. Although its mechanism is unclear, POI symptoms are known to be caused by inflammation 6 to 72 h after surgery. As proton pump inhibitors exhibit protective effect against acute inflammation, the purpose of this study was to determine the effect of ilaprazole on a POI rat model. POI was induced in rats by abdominal surgery. Rats were divided into six groups: control: normal rat + 0.5% CMC-Na, vehicle: POI rat + 0.5% CMC-Na, mosapride: POI rat + mosapride 2 mg/kg, ilaprazole 1 mg/kg: POI rat + ilaprazole 1 mg/kg, ilaprazole 3 mg/kg: POI rat + ilaprazole 3 mg/kg, and ilaprazole 10 mg/kg: POI rat + ilaprazole 10 mg/kg. Gastrointestinal motility was confirmed by measuring gastric emptying (GE) and gastrointestinal transit (GIT). In the small intestine, inflammation was confirmed by measuring TNF-α and IL-1β; oxidative stress was confirmed by SOD, GSH, and MDA levels; and histological changes were observed by H&E staining. Based on the findings, GE and GIT were decreased in the vehicle group and improved in the ilaprazole 10 mg/kg group. In the ilaprazole 10 mg/kg group, TNF-α and IL-1β levels were decreased, SOD and GSH levels were increased, and MDA levels were decreased. Histological damage was also reduced in the ilaprazole-treated groups. These findings suggest that ilaprazole prevents the decrease in gastrointestinal motility, a major symptom of postoperative ileus, and reduces inflammation and oxidative stress.

When the skin and soft tissue necrosis occurs due to extravasation of intravenously administrated biological active materials and drugs, no specific mode of treatment modality is known except for supportive management or debridement and skin graft. This experiment was designed to determine the effective dosage of hyaluronidase and triamcinolone acetonide on the extravasation necrosis caused by calcium gluconate and to establish the optimal time of administration of the antidotes. Initially 0.4 ml of 10% calcium gluconate was injected subcutaneously into the rabbit back. Study I was designed to observe the skin change in 8 groups including control group with no treatment and treated groups with normal saline, saline with hyaluronidase(dosage: 150, 300, 600 unit), saline with triamcinolone acetonide(1 mg, 2 mg), and 150 unit hyaluronidase and 1 mg triamcinolone acetonide (all in volume 0.2 ml, treatment delay: immediate, 15-minutes, 30-minutes, 1-hour, 3-hours delay). The sizes of skin necrosis and induration were measured and compared between each group. Study II was designed to examine the histologic findings of the skin and evaluate the effect of hyaluronidase and triamcinolone acetonide on tissue damage. The sizes of induration and necrosis are smaller in all treated groups than non-treated group and the statistically significant protective effect on reducing the size of necrosis was found in groups treated with the drugs within 15 minutes to 30 minutes(p < 0.05). The most effective protection was obtained by the immediate injection of 150 unit dosage of hyaluronidase with 1 mg triamcinolone acetonide. This study suggests that intralesional injection of hyaluronidase and triamcinolone acetonide within half hour delay for the treatment of extravasation necrosis of calcium gluconate is the most effective, probably due to their diffusion, antiinflammatory effect and role in facilitating the resorption of calcium in the tissue.
Antidotes ; Calcium Gluconate* ; Calcium* ; Debridement ; Diffusion ; Hyaluronoglucosaminidase* ; Injections, Intralesional ; Necrosis ; Skin ; Transplants ; Triamcinolone Acetonide* ; Triamcinolone*