Background: General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods: A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results: In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.

Background: General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods: A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results: In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.

Background: General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods: A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results: In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.

Background: General anesthesia is inevitable for pediatric patients undergoing surgery, though volatile anesthetic agents may cause neuroinflammation and neurodevelopmental impairment; however, the underlying pathophysiology remains unclear. We aimed to investigate the neuroinflammation mechanism in developing rat brains associated with sevoflurane exposure time, by identifying the specific damage-associated molecular patterns (DAMPs) pathway and evaluating the effects of non-steroidal anti-inflammatory drugs (NSAIDs) in alleviating neuroinflammation. Methods: A three-step experiment was conducted to investigate neuroinflammation induced by sevoflurane. First, the exposure time required for sevoflurane to cause neuroinflammation was determined. Next, the specific pathways of DAMPs involved in neuroinflammation by sevoflurane were identified. Finally, the effects of NSAIDs on sevoflurane-induced neuroinflammation were investigated. The expression of various molecules in the rat brain were assessed using immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay. Results: In total, 112 rats (aged 7 days) were used, of which six rats expired during the experiment (mortality rate, 5.3%). Expression of CD68, HMGB-1, galectin-3, TLR4, TLR9, and phosphorylated NF-κB was significantly increased upon 6 h of sevoflurane exposure. Conversely, transcriptional levels of TNF-α and IL-6 significantly increased and IFN-γ significantly decreased after 6 h of sevoflurane exposure. Co-administration of NSAIDs with sevoflurane anesthesia significantly attenuated TNF-α and IL-6 levels and restored IFN-γ levels. Conclusions In conclusion, 6 h of sevoflurane exposure induces neuroinflammation through the DAMPs pathway, HMGB-1, and galectin-3. Co-administration of ibuprofen reduced sevoflurane-induced neuroinflammation.

Recently vesicovaginal fistula is rare, but infrequently is found after pelvic surgery especially total hysterectomy for benign gynecologic diseases. In general, the correction of vesicovaginal fistula has been performed 3-4 months after the diagnosis. Recently, earlier correction of fistula was challenged. It has been reported that Latzko operation is a simple effective method for easy correction of vesicovaginal fistula in early correction. We experienced two successful cases of Latzko operation, which were performed as early as day 25 and 31 postoperatively.
Diagnosis ; Female ; Fistula ; Genital Diseases, Female ; Hysterectomy* ; Vesicovaginal Fistula*

OBJECTIVES: The aim of this study was to evaluate the associations between vasomotor symptoms and factors such as sociodemographics, health behaviors, medical condition, depression, stress, anxiety, attitude toward menopause, and quality of life. METHODS: We conducted a cross-sectional study in peri- and post-menopausal women enrolled by the Korean Association of Health Promotion. Subjects submitted self-report questionnaires about vasomotor symptoms and other clinical symptoms. Associations between vasomotor symptoms and clinical variables were analyzed using stepwise multiple regression analyses. RESULTS: 1951 women completed self-report questionnaires and 1022 women were enrolled in the study. The prevalence of vasomotor symptoms in peri- and post-menopausal women was 63.9%. Variables showing significant differences between subjects with vasomotor symptoms and subjects without them were score of Beck Depression Inventory, Brief Encounter Psychosocial Instrument-Korean Version, proportions of clinically significant depression(Beck Depression Inventory≥16), Menopausal rating scale, attitude towards menopause, the 4 subscales of World Health Organization Quality of Life-BREF(Physical health, psychological, social relationships, environment), and a History of Premenstrual syndrome/Premenstrual dysphoric disorder. Stepwise multiple regression analyses indicated that Beck Depression Inventory, Brief Encounter Psychosocial Instrument-Korean Version, Menopausal Rating Scale, and the Psychological subscale of World Health Organization Quality of Life -BREF show associations with vasomotor symptoms. CONCLUSIONS: Menopausal vasomotor symptoms are associated with various psychological factors, especially with depression. Midlife women suffering vasomotor symptoms should therefore be screened for depression. Future prospective studies where clinical subjects are diagnosed using structured interviews, focusing on the causal relationship between depression and vasomotor symptoms are necessary.
Anxiety ; Cross-Sectional Studies ; Depression* ; Female ; Health Behavior ; Health Promotion ; Humans ; Menopause ; Prevalence ; Prospective Studies ; Psychology ; Quality of Life* ; World Health Organization

PURPOSE: We evaluated the correlation between correction angle and pain of the first metatarsophalangeal joint in the treatment of hallux valgus. MATERIALS AND METHODS: The 28 cases (20 patients) with moderate to severe hallux valgus deformity and pain of the first metatarsophalangeal joint who underwent the distal soft tissue procedure and proximal metatarsal closing wedge osteotomy, were divided into two groups, Group I: no pain of the first metatarsophalangeal joint after surgery, and Group II: with persisting pain. We analyzed the correc-tion angle and pain of the first metatarsophalangeal joint in each group, preoperatively and at the last follow-up. All of the patients were women and their mean age was 58 years old. The average follow-up time was 18 months. RESULTS: At the last follow-up, the 21 feet (75%) were free of pain of the first metatarsophalangeal joint. In 7 feet (25%) pain persisted. In group I, sufficient deformity correction was obtained, but in group II, the deformity was corrected insufficiently. A high correlation was observed between correction angle and pain relief. CONCLUSION: A high correlation was obtained between correction angle and pain of the first metatarsophalangeal joint in the treatment of hallux valgus deformity. Therefore, in view of the patient's expectation of pain relief, meticulous attention should be paid to the correction of hallux valgus deformity.
Congenital Abnormalities ; Female ; Follow-Up Studies ; Foot ; Hallux Valgus* ; Hallux* ; Humans ; Metatarsal Bones ; Metatarsophalangeal Joint* ; Middle Aged ; Osteotomy

BACKGROUND: Postoperative nausea and vomiting (PONV) is a common problem in patients undergoing thyroidectomy. In this study we evaluated the effects of prophylactic dolasetron and/or induction with propofol on PONV. METHODS: Two hundred three patients scheduled thyroidectomy under general anesthesia with sevoflurane were included and were randomly allocated to one of four groups. In control (group C) and dolasetron groups (group D), the patients received thiopental sodium 4-5 mg/kg intravenously for the induction of anesthesia, and the patients in group D received prophylactic intravenous dolasetron 210 microgram/kg. In propofol (group P) and dolasetron + propofol groups (group D + P), the patients received propofol 2 mg/kg intravenously for the induction of anesthesia, and the patients in group D + P received prophylactic intravenous dolasetron 210 microgram/kg. The incidence and severity of PONV, the need for rescue antiemetics, adverse events were assessed during 0 to 1 hour and 1 to 24 hours postoperatively. RESULTS: During the first 24 hours after anesthesia, the incidences of PONV and postoperative vomiting were significantly reduced in group D + P compared with group C (P < 0.05, respectively). There were no significant differences in postoperative nausea, need for rescue antiemetics, severity of PONV, and adverse events of antiemetics among the four groups. CONCLUSIONS: In patients with thyroidectomy, combination of prophylactic dolasetron administration and induction with propofol was found to reduce the incidence of PONV during the first 24 hours after anesthesia, compared with that of routine induction with thiopental sodium.
Anesthesia ; Anesthesia, General ; Antiemetics ; Humans ; Incidence ; Indoles ; Methyl Ethers ; Postoperative Nausea and Vomiting ; Propofol ; Quinolizines ; Thiopental ; Thyroidectomy

BACKGROUND: More than half of the causes of male osteoporosis is due to secondary osteoporosis. Therefore, it is important to detect and modify its related factors. The aim of this study was to find related lifestyle factors and biochemical markers with low bone mineral density (BMD) in Korean men. METHODS: A cross-sectional analysis was performed in men aged 40-69 years who visited a hospital for health checkup from January to March 2007. BMD was measured at proximal femur and lumbar spine by dual energy x-ray absorptionmetry. Lifestyle factors were estimated by a self-administered questionnaire and fasting glucose, uric acid, gamma glutamyltransferase, alkaline phosphatase, creatinine, free testosterone, 25-OH vitamin D, urine deoxypyridinoline, osteocalcin were measured. Multivariate logistic regression was used to find the association to the lowest tertile of BMD. RESULTS: A total of 152 subjects were included. After multivariate analysis adjusted with age, BMI, smoking, alcohol and exercise, different factors were correlated with low bone density in each site of femoral neck and lumbar spine. Factors correlated at both sites were BMI and exercise; lower BMI and doing no exercise increased risks of low bone density. Increasing age and alcohol intake > or = 14 drinks/week were associated with lower BMD at femoral neck. The factors associated with lower lumbar spine BMD only were lower level of uric acid and higher level of urine deoxypyridinoline. CONCLUSION: Different factors were associated with low bone density at femoral neck and lumbar spine in men. BMI and exercise were related in both sites; age, alcohol intake, uric acid and deoxypyridinoline were related on either site.
Adult ; Aged ; Alcohol Drinking ; Alkaline Phosphatase ; Amino Acids ; Biomarkers ; Bone Density ; Creatinine ; Cross-Sectional Studies ; Fasting ; Femur ; Femur Neck ; gamma-Glutamyltransferase ; Glucose ; Health Behavior ; Humans ; Life Style ; Logistic Models ; Male ; Multivariate Analysis ; Osteocalcin ; Osteoporosis ; Smoke ; Smoking ; Spine ; Testosterone ; Uric Acid ; Vitamin D ; Surveys and Questionnaires

Spontaneous coronary artery dissection (SCAD) is an extremely rare clinical manifestation of ischemic heart disease. A 43-year-old female was admitted to our hospital for non-ST elevation myocardial infarction. She had no cardiac risk factors except smoking. Coronary angiography showed moderate stenosis of the proximal left circumflex artery (LCX) with intraluminal haziness and a spastic appearance from the culprit lesion in the left main coronary artery (LM). Subsequent analysis by intravascular ultrasound (IVUS) revealed a clear dissection flap from the LCX to the LM. Generally, SCAD of the LM or multivessel involvement requires primary surgical management. The present case was treated percutaneously using the culotte stent technique.
Adult ; Arteries ; Constriction, Pathologic ; Coronary Angiography ; Coronary Disease ; Coronary Vessels ; Female ; Humans ; Muscle Spasticity ; Myocardial Infarction ; Myocardial Ischemia ; Risk Factors ; Smoke ; Smoking ; Stents