Background: Tibial tuberosity transposition (TTT) causes caudalization of the patellar ligament insertion in canine medial patellar luxation, which can lead to increases in patellofemoral contact pressure. Objectives: The purpose of this study is to confirm the effect of patellofemoral contact mechanics after craniolateral and caudolateral transposition of tibial tuberosity in normal canine hindlimbs. Methods: Craniolateral and caudolateral transposition of tibial tuberosity was performed in 5 specimens, respectively. The pressure was measured in the specimen before TTT, and then in the same specimen after TTT. In this process, data was obtained in 10 specimens. The measurement results were output as visualization data through the manufacturer's software and numerical data through spreadsheet. Based on these 2 data and the anatomical structure of the patellofemoral joint (PFJ) surface, whole measurement area was analysed by dividing into medial, lateral and central area. Results: In craniolateralization of tibial tuberosity, total, medial, central contact pressure was decreased and lateral contact pressure was not statistically changed lateral contact pressure than normal PFJ. In caudolateralization of tibial tuberosity, total, lateral contact pressure was increased and medial contact pressure was not statistically changed than normal PFJ. Although not statistically significant changed, central contact pressure in caudolateralization of tibial tuberosity was increased in all 5 specimens. Conclusions These results imply that traditional TTT, prone to caudal shift of patellar tendon, can increase retropatellar pressure may lead to various complications and diseases of the stifle joint.

No abstract available.
Caves ; Esophageal and Gastric Varices ; Portal Vein

Background: Postoperative pain is affected by preoperative depression. If the risk of postoperative pain associated with depression can be predicted preoperatively, anesthesiologists and/or surgeons can better manage it with personalized care. The objective of this study was to determine the efficacy of Patient Health Questionnaire-2 (PHQ-2) depression screening tool as a predictor of postoperative pain. Methods: A total of 50 patients scheduled for elective laparoscopic cholecystectomy with an American Society of Anesthesiologists grade of 1 or 2 were enrolled. They answered the PHQ-2, which consists of two questions, under the supervision of a researcher on the day before the surgery. The numerical rating scale (NRS) scores were assessed at post-anesthesia care unit (PACU), at 24, and 48 postoperative hours, and the amount of intravenous patient-controlled analgesia (IV-PCA) administered was documented at 24, 48, and 72 postoperative hours. At 72 h, the IV-PCA device was removed and the final dosage was recorded. Results: The NRS score in PACU was not significantly associated with the PHQ-2 score (correlation coefficients: 0.13 [P = 0.367]). However, the use of analgesics after surgery was higher in patients with PHQ-2 score of 3 or more (correlation coefficients: 0.33 [P = 0.018]). Conclusions We observed a correlation between the PHQ-2 score and postoperative pain. Therefore, PHQ-2 could be useful as a screening test for preoperative depression. Particularly, when 3 points were used as the cut-off score, the PHQ-2 score was associated with the dosage of analgesics, and the analgesic demand could be expected to be high with higher PHQ-2 scores.

Background: There are several advantages of low flow anesthesia including safety, economics, and eco-friendliness. However, oxygen concentration of fresh gas flow and inspired gas are large different in low flow anesthesia. This is a hurdle to access to low flow anesthesia. In this study, we aimed to investigate the change in inhaled oxygen concentration in low flow anesthesia using oxygen and medical air. Methods: A total of 60 patients scheduled for elective surgery with an American Society of Anesthesiologist physical status I or II were enrolled and randomly allocated into two groups. Group H: Fresh gas flow rate (FGF) 4 L/min (FiO₂ 0.5). Group L: FGF 1 L/min (FiO₂ 0.5). FGF was applied 4 L/min in initial phase (10 min) after intubation. After initial phase FGF was adjusted according to groups. FGF continued at the end of surgery. Oxygen and inhalation anesthetic gas concentration were recorded for 180 min at 15 min interval. Results: The inspired oxygen concentration decreased by 5.5% during the first 15 min in the group L. Inspired oxygen decreased by 1.5% during next 15 min. Inspired oxygen decreased by 1.4% for 30 to 60 min. The inspired oxygen of group L is 35.4 ± 4.0% in 180 min. The group H had little difference in inspired oxygen concentration over time and decreased by 1.8% for 180 min. Conclusions The inspired oxygen concentration is maintained at 30% or more for 180 min in patients under 90 kg. Despite some technical difficulties, low flow anesthesia may be considered.

PURPOSE: Phenylbutyrate is an effective redifferentiating agent in several human cancers. Recently phenylbutyrate has been reported to inhibit histone deacetylase activity. We investigated the effects of sodium 4-henylbutyrate (Na-4-PB) on cell proliferation in a human pancreatic cancer cell line. METHODS: A human pancreatic cancer cell line, Aspc-1 was purchased from Korean Cell Line Bank. Antiproliferative effects of sodium 4-phenylbutyrate were measured by MTT assay and their mechanisms were evaluated by apoptosis assay and cell cycle analysis. RESULTS: After 3 days of treatment with Na-4-PB at the concentration of 2.5, 5, 7.5, and 10 mM, relative growth inhibition compared to control was 21.3+/-8.3% (mean+/-SD), 37.8+/-2.3%, 46.7+/-0.5%, and 56.7+/-1.7% respectively (p < 0.05). Antiproliferative effect of Na-4-PB was also time-dependent. Combination treatment with Na-4-PB and troglitazone, a PPARg agonist, increased antiproliferative effects but was not synergistic. After 48 hour treatment with Na-4-PB, early apoptotic cell population in control, 2.5, and 5 mM of Na-4-PB was 29.6%, 44.2%, and 65.9%, respectively. After 24 hour treatment with Na-4- PB, G0/G1 phase population in control, 2.5, and 5 mM of Na-4-PB was 55.0%, 67.4%, and 65.8%, respectively. CONCLUSION: Na-4-PB inhibited pancreatic cancer cell proliferation by inducing apoptosis and cell cycle arrest at G0/G1 phase in time- and dose-dependent manner. Combination treatment with Na-4-PB and other chemotherapeutic agents such as troglitazone, a PPARg agonist, can enhance antiproliferative effects. Na-4-PB might be a promising potential therapeutic agent for patients with pancreatic cancer.
Apoptosis ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line* ; Cell Proliferation ; Histone Deacetylases ; Humans ; Pancreatic Neoplasms* ; Sodium

BACKGROUND/AIMS: The optimal strategy for anticoagulation treatment in patients with atrial fibrillation (AF) and end-stage renal disease (ESRD) has not been established. We evaluated the efficacy and bleeding risk of warfarin and antiplatelet agents in patients with AF and ESRD. METHODS: We retrospectively reviewed the medical records of 256 patients with AF and ESRD and included 158 patients (age, 63.7 ± 12.2 years; male sex, n = 103) with a CHA2DS2-VASc score ≥ 1 who were taking warfarin (n = 53) or an antiplatelet agent (n = 105). RESULTS: During the follow-up period (31.0 ± 29.4 months), 10 ischemic events and 29 major bleeding events occurred. The thromboembolic event rate did not significantly differ between the warfarin and antiplatelet groups (1.9% and 8.6%, respectively; p = 0.166). However, the rate of major bleeding events was significantly higher in the warfarin group than it was in the antiplatelet group (32.1% and 11.4%, respectively; p = 0.002). Cox's regression analysis indicated that warfarin was related to an increased risk of major bleeding events (hazard ratio [HR], 3.44; 95% confidence interval [CI], 1.60–7.36; p = 0.001). Conversely, warfarin was not related to a decreased risk of thromboembolic events (HR, 0.34; 95% CI, 0.04–2.70; p = 0.306). CONCLUSIONS: In patients with AF and ESRD, warfarin use was associated with an increased risk of bleeding events, compared with antiplatelet agents.
Anticoagulants ; Atrial Fibrillation ; Follow-Up Studies ; Hemorrhage ; Humans ; Kidney Failure, Chronic ; Male ; Medical Records ; Platelet Aggregation Inhibitors ; Retrospective Studies ; Warfarin

BACKGROUND/AIMS: The optimal strategy for anticoagulation treatment in patients with atrial fibrillation (AF) and end-stage renal disease (ESRD) has not been established. We evaluated the efficacy and bleeding risk of warfarin and antiplatelet agents in patients with AF and ESRD. METHODS: We retrospectively reviewed the medical records of 256 patients with AF and ESRD and included 158 patients (age, 63.7 ± 12.2 years; male sex, n = 103) with a CHA2DS2-VASc score ≥ 1 who were taking warfarin (n = 53) or an antiplatelet agent (n = 105). RESULTS: During the follow-up period (31.0 ± 29.4 months), 10 ischemic events and 29 major bleeding events occurred. The thromboembolic event rate did not significantly differ between the warfarin and antiplatelet groups (1.9% and 8.6%, respectively; p = 0.166). However, the rate of major bleeding events was significantly higher in the warfarin group than it was in the antiplatelet group (32.1% and 11.4%, respectively; p = 0.002). Cox's regression analysis indicated that warfarin was related to an increased risk of major bleeding events (hazard ratio [HR], 3.44; 95% confidence interval [CI], 1.60–7.36; p = 0.001). Conversely, warfarin was not related to a decreased risk of thromboembolic events (HR, 0.34; 95% CI, 0.04–2.70; p = 0.306). CONCLUSIONS In patients with AF and ESRD, warfarin use was associated with an increased risk of bleeding events, compared with antiplatelet agents.

BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS: There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.
Anesthesia, Spinal ; Bradycardia ; Dexmedetomidine ; Heart Rate ; Heart ; Humans ; Hypnotics and Sedatives ; Operating Rooms

BACKGROUND: Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. METHODS: The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. RESULTS: During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). CONCLUSIONS There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.