PURPOSE: While the rate of breast-feeding has been rising recently in many countries, it has been gradually falling in Korea. Accordingly, we took a survey in Jeon-ju to discover the actual state of breast-feeding and find a solution. METHODS: Eight hundred and sixty-four questionnaires of filled out by mothers who visited the seven local pediatric clinics and the clinic of pediatric department in the Presbyterian Medical Center(PMC) in Jeon-ju from January 1998 to June 1998 were analysed by ANOVA, cross analysis, frequency analysis and correlation analysis using SPSS program. RESULTS: In the case of six-months-old babies, the breast-feeding rate was 35.6%. The breast-feeding rate was higher when it came to a normal delivery, and was also related to the inperiority of infant birth order and lack of maternal academic background(P<0.05). The main reasons to switch from successful breast-feeding to formula-feeding before 6 months of age were insufficient breast-milk(49.3%). The survey shows the best thing for a infant's health is breast milk (86.0%). CONCLUSION: In order to increase the rate of breast-feeding, it's essential to educate people in school and it is necessary to create a hospital environment in which mothers can easily begin breast-feeding as soon as possible after delivery.
Birth Order ; Humans ; Infant ; Jeollabuk-do* ; Korea ; Milk, Human ; Mothers ; Protestantism ; Surveys and Questionnaires

OBJECTIVE: We investigated the neuroprotective effect of anthocyanin, oxygen radical scavenger extracted from raspberries, after traumatic spinal cord injury (SCI) in rats. METHODS: The animals were divided into two groups : the vehicle-treated group (control group, n=20) received an oral administration of normal saline via stomach intubation immediately after SCI, and the anthocyanin-treated group (AT group, n=20) received 400 mg/kg of cyanidin 3-O-beta-glucoside (C3G) in the same way. We compared the neurological functions, superoxide expressions and lesion volumes in two groups. RESULTS: At 14 days after SCI, the AT group showed significant improvement of the BBB score by 16.7+/-3.4%, platform hang by 40.0+/-9.1% and hind foot bar grab by 30.8+/-8.4% (p<0.05 in all outcomes). The degree of superoxide expression, represented by the ratio of red fluorescence intensity, was significantly lower in the AT group (0.98+/-0.38) than the control group (1.34+/-0.24) (p<0.05). The lesion volume in lesion periphery was 32.1+/-2.4 microL in the control and 24.5+/-2.3 microL in the AT group, respectively (p<0.05), and the motor neuron cell number of the anterior horn in lesion periphery was 8.3+/-5.1 cells/HPF in the control and 13.4+/-6.3 cells/HPF in the AT group, respectively (p<0.05). CONCLUSION: Anthocyanin seemed to reduce lesion volume and neuronal loss by its antioxidant effect and these resulted in improved functional recovery.
Administration, Oral ; Animals ; Anthocyanins ; Antioxidants ; Cell Count ; Fluorescence ; Foot ; Horns ; Intubation ; Motor Neurons ; Neurons ; Neuroprotective Agents ; Oxygen ; Spinal Cord ; Spinal Cord Injuries ; Stomach ; Superoxides

Among nondepolarizing neuromuscular blocking agents, d-tubocurarine may cause blood pressure reduction due to ganglionic blockade and histamine release, while pancuronium and gallamine are associated with vagal blockade and heart rate acceleration. Metocurine, as a trimethylated derivative of d-tubocurarine synthesized by King in 1935, is known to have relatively long duration of action and produces little change in cardiovascular system. Despite its relative lack of cardiovascular effects, the accumulation of data with regard to human neuromus- cular pharmacology and the clinical use has been scant. One hundred and nine adult patients of either sex were anesthetized with thiopental sodium and 50% nitrous oxide with 1.5-2.5% enflurane. For evaluation of neuromuscular blocking effect of metocurine, train-of-four stimulation (2.0 Hz for 2 seconds) was applied at the wrist along the ulnar nerve distribution and the response was measured via ABM Datex. Systolic, diastolic blood pressure and heart rate were recorded continuously after administration of metocurine, d-tubocurarine or pancuronium. All data were analized by ANOVA, Scheffe test. The results are follows : 1) The mean onset times of metocurine 0.1, 0.2, 0.3 mg/kg groups were 119.5+/-40.0, 120.9+/-61.1, 84.8+/-61,1 seconds and the mean durations were 75.1+/-37.6, 104.9+/-42.1, 131.0+/-42.5 minutes respectively. 2) Single-bolus dose of metocurine 0.1, 0.2, and 0.3 mg/kg did not cause significant cardiovascular changes from the control values, but d-tubocurarine 0.3 mg/kg decreased mean systolic blood pressure significantly from 116.6+/-15.7 to 99.0+/-10.9 mmHg 2 minutes after injection. 3) Systolic blood pressures of metocurine 0.2 mg/kg (107.2+/-11.7 mmHg) and d-tubocurarine 0.3 mg/ kg (100.4+/-12.9 mmHg) were significantly different from that of pancuronivm 0.06 mg/kg (127.8+/-16. 0 mmHg) after 1 minute, and 2 minutes after injection, systolic blood pressure of metocurine 0.2 mg/ kg (110.2+/-14.3 mmHg) and d-tubocurarine 0.3 mg/kg (99.0+/-10.9 mmHg) were different from that of pancuronium 0.06 mg/kg (125.3+13.1 mmHg). Five minutes after injection, systolic pressure of d- tubocurarine 0.3mg/kg group (101.110.2mmHg) was significantly different from that of pancur-onium 0.06 mg/kg group (118.7+/-11.0 mmHg). 4) Diastolic blood pressure of d-tubocurarine 0.3 mg/kg (63.4+/-12.9 mmHg) was significantly differ- ent from that of pancuronium 0.06mg/kg (84.2+/-13.3mmHg) after 1 minute, and 2 minutes after injection, diastolic blood pressure or d-tubocurarine 0.3 mg/kg (65.4+/-11.3 mmHg) was different from that of pancuronium 0.06mg/kg (83.1+/-11.6mmHg). There was no significant difference among the groups with respect to heart rate. In summary, metocurine has relatively rapid onset and long duration of action, and used in a dose sufficient to provide surgical relaxation, it produces little change in cardiovascular system in contrast to d-tubocurarine or pancuronium. 1t is therefore suggested that metocurine may be recommended as a muscle relaxant for patients having cardiovascular disease.
Acceleration ; Adult ; Blood Pressure ; Cardiovascular Diseases ; Cardiovascular System ; Enflurane ; Gallamine Triethiodide ; Ganglion Cysts ; Heart Rate ; Hemodynamics* ; Histamine Release ; Humans ; Neuromuscular Blockade* ; Neuromuscular Blocking Agents ; Nitrous Oxide ; Pancuronium ; Pharmacology ; Relaxation ; Thiopental ; Tubocurarine ; Ulnar Nerve ; Wrist

BACKGROUND: Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IkappaBalpha)/nuclear factor-kappa B (NF-kappaB) pathway in RAW 264.7 cells. METHODS: Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IkappaBalpha and nuclear translocation of NF-kappaB p65 were measured by Western blotting, and IkappaB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IkappaBalpha/NF-kappaB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment. RESULTS: The increase of IL-6 and TNF-alpha in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IkappaBalpha degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-kappaB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IkappaBalpha degradation and NF-kappaB transcription by AVP was abolished by tolvaptan treatment. CONCLUSIONS: Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IkappaBalpha/NF-kappaB cascade in mouse macrophages via V2 receptors.
Animals ; Antigen-Antibody Complex ; Arginine Vasopressin ; Blotting, Western ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; I-kappa B Kinase ; Interleukin-6 ; Macrophages ; Mice ; NF-kappa B ; Phosphotransferases ; Receptors, Vasopressin ; Tumor Necrosis Factor-alpha

In this study, we explored the potentiality of human arginine decarboxylase (ADC) to enhance the survival of mesenchymal stem cells (MSCs) against unfavorable milieu of host tissues as the low survival of MSCs is the issue in cell transplantation therapy. To address this, human MSCs overexpressing human ADC were treated with H2O2 and the resultant intracellular events were examined. First, we examined whether human ADC is overexpressed in human MSCs. Then, we investigated cell survival or death related events. We found that the overexpression of human ADC increases formazan production and reduces caspase 3 activation and the numbers of FITC, hoechst, or propidium iodide positive cells in human MSCs exposed to H2O2. To elucidate the factors underlying these phenomena, AKT, CREB, and BDNF were examined. We found that the overexpression of human ADC phosphorylates AKT and CREB and increases BDNF level in human MSCs exposed to H2O2. The changes of these proteins are possibly relevant to the elevation of agmatine. Collectively, our data demonstrate that the overexpression of human ADC stimulates pro-survival factors to protect human MSCs against H2O2 toxicity. In conclusion, the present findings support that ADC can enhance the survival of MSCs against hostile environment of host tissues.
Apoptosis/*drug effects ; Brain-Derived Neurotrophic Factor/metabolism ; Carboxy-Lyases/genetics/*metabolism ; Caspase 3/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Humans ; Hydrogen Peroxide/*toxicity ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/cytology/drug effects/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism

Neural stem cells (NSCs) have been suggested as a groundbreaking solution for stroke patients because they have the potential for self-renewal and differentiation into neurons. The differentiation of NSCs into neurons is integral for increasing the therapeutic efficiency of NSCs during inflammation. Apoptosis signal-regulating kinase 1 (ASK1) is preferentially activated by oxidative stress and inflammation, which is the fundamental pathology of brain damage in stroke. ASK1 may be involved in the early inflammation response after stroke and may be related to the differentiation of NSCs because of the relationship between ASK1 and the p38 mitogen-activated protein kinase pathway. Therefore, we investigated whether ASK1 is linked to the differentiation of NSCs under the context of inflammation. On the basis of the results of a microarray analysis, we performed the following experiments: western blot analysis to confirm ASK1, DCX, MAP2, phospho-p38 expression; fluorescence-activated cell sorting assay to estimate cell death; and immunocytochemistry to visualize and confirm the differentiation of cells in brain tissue. Neurosphere size and cell survival were highly maintained in ASK1-suppressed, lipopolysaccharide (LPS)-treated brains compared with only LPS-treated brains. The number of positive cells for MAP2, a neuronal marker, was lower in the ASK1-suppressed group than in the control group. According to our microarray data, phospho-p38 expression was inversely linked to ASK1 suppression, and our immunohistochemistry data showed that slight upregulation of ASK1 by LPS promoted the differentiation of endogenous, neuronal stem cells into neurons, but highly increased ASK1 levels after cerebral ischemic damage led to high levels of cell death. We conclude that ASK1 is regulated in response to the early inflammation phase and regulates the differentiation of NSCs after inflammatory-inducing events, such as ischemic stroke.
Animals ; Cell Death ; Infarction, Middle Cerebral Artery/*metabolism ; Lipopolysaccharides/pharmacology ; MAP Kinase Kinase Kinase 5/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neural Stem Cells/cytology/drug effects/*metabolism ; *Neurogenesis ; Neuropeptides/genetics/metabolism ; p38 Mitogen-Activated Protein Kinases/genetics/metabolism

OBJECTIVE: Chronic subdural hematoma (CSDH), a disease commonly encountered by neurosurgeons, is treated by burr hole drainage (BHD). However, the optimal surgical technique among the three types of BHD has not been determined. METHODS: We conducted a retrospective study on BHD performed on 93 patients who were diagnosed with CSDH. The subjects were divided into three groups based on the surgical technique performed: single BHD without irrigation (Group A, n=31), double BHD without irrigation (Group B, n=32), and double BHD with irrigation (Group C, n=30). The clinical factors, radiological factors and recurrences were compared between the three groups. Moreover, independent factors affecting the recurrence were analyzed. RESULTS: The change in hematoma thickness was 29.77+/-7.94%, 49.73+/-12.87%, and 75.29+/-4.32% for Group A, B, and C, respectively, while the change in midline shift was 40.81+/-15.47%, 51.78+/-10.94%, and 56.16+/-16.16%, respectively. Thus, Group C showed the most effective for resolution of hematoma and midline shift (p<0.05). Group A, B, and C had 12 cases (38.7%), 8 cases (25.0%), and 3 cases (10.0%) of recurrences, respectively. Group C had a statistically significantly fewer recurrence rate than Group A (p<0.05). Double burr hole, irrigation, and coagulopathy were each identified as independent factors that reduce recurrence (p<0.05). CONCLUSION: Among the three techniques, the double BHD with saline irrigation resulted in the fewest recurrences. It is probably the most effective technique for preventing the recurrence of CSDH.
Drainage* ; Hematoma ; Hematoma, Subdural, Chronic* ; Humans ; Recurrence* ; Retrospective Studies ; Therapeutic Irrigation ; Trephining

A 24 years old female patient presented for surgical resection of a large chemodectoma with extensive involvement of the bifurcation of the left common carotid artery. Anesthesia was induced with thiopental and maintained with 0.75~1.25% halothane with 50% nitrous oxide in oxygen. Arterial blood pressure and carbon dioxide tension were maintained at preoperative levels with a direct arterial pressure monitoring device and an ABM end-tidal carbon dioxide monitoring device. Thiopental was infused continuously by a microinfusion pump(2mg/kg/hr) during the procedure and an intraluminal shunt was inserted in the left internal carotid artery to protect the brain form hypoxic attack. Body temperature was monitored and electrocardiography and electroencephalography were also applied. No significant changes in vital signs and electroencephalgraphy during anesthesia were noted with the exception of a temporary decreas in blood pressure due to bleeding from the accidental perforation of the left internal carotid artery. The patient responded soon after the withdrawal of anesthesia and she was discharged from hospital with an uneventful recovery on the seventh postoperative day. A reduction in cerebral blood flow without a concomitant reduction in cerebral metabolic rate during carotid arterial procedures may result in significant neurologic derangements. Therefore, the major role of the anesthesiologist is the maintenance of adequate oxygen delivery to the brain and the reduction of cerebral metabolic demands.
Anesthesia ; Arterial Pressure ; Blood Pressure ; Body Temperature ; Brain ; Carbon Dioxide ; Carotid Arteries* ; Carotid Artery, Common ; Carotid Artery, Internal ; Electrocardiography ; Electroencephalography ; Female ; Halothane ; Hemorrhage ; Humans ; Nitrous Oxide ; Oxygen ; Paraganglioma, Extra-Adrenal ; Thiopental ; Vital Signs ; Young Adult

BACKGROUND: In order to evaluate the effects of the duration of hemodialysis on cell mediated immunity, we studied cellular immune responses in vitro in 12 patients on chronic hemodialysis and in 6 healthy volunteers with normal kidney function. METHODS: The patients on maintenance hemodialysis were divided into two subgroups according to the duration of the hemodialysis: Group 1 (within 5 years, n=6) and Group 2 (>5 yr and < or =10 yr, n=6). Group 3 include the normal control (n=6). The peripheral blood lymphocytes of each group were cultured in RPMI medium 1640 without/or with 3 microgram of phytohemagglutinin (=PHA) for 7 days. RESULTS: CD4 /CD8 ratio at 48hours was totally comparable between the uremic patients (Group 1 and Group 2) and the controls (Group 3). The proportions of CD25 T lymphocytes after 48 hours culture were abnormally high: 7.1+/-0.5% and 7.0+/-1.3% in the uremic patients as compared to 2.5+/-0.6 in the normal controls at the basal state and 66.7+/-2.6% and 68.8+/-1.9% in the uremic patients as compared to 78.3+/-4.6% in the normal controls at the PHA-stimulated condition. The spontaneous production of IL-2 (mean pg SEM) was significantly lower in hemodialized patients (Group 1: 34.5+/-6.0 pg/ml, Group 2: 33.8+/-6.2 pg/ml) as compared to the normal patients (Group 3: 58.8+/-10.4 pg/ml). The PHA stimulated IL-2 production was also significantly reduced in the hemodialized patients (Group 1: 53.2+/- 13.3 pg/ml, Group: 53.0+/-10.3 pg/ml) as compared to the normal patients (Group 3: 150.0+/-24.5 pg/ml). The mean proliferative response to PHA at each point in the hemodialized patients were significantly lower than those of the controls. CONCLUSIONS: These data show that there is no significant correlation between the level of the cell mediated immune response and the duration of hemodialysis. Several defects in the cell mediated immune response associated with uremia might start at an early phase of the hemodialysis.
Healthy Volunteers ; Humans ; Immunity, Cellular* ; Interleukin-2 ; Kidney ; Kidney Failure, Chronic* ; Lymphocytes ; Renal Dialysis* ; T-Lymphocytes ; Uremia

BACKGROUND: Portable glucometers are often utilized at the patient's bedside in the ICU or operating room for frequent measurements of the blood glucose concentration. Many of these devices are based on a glucose oxidase method that may be influenced by PO2. The aim of this study was to evaluate the influence of a high PO2 of arterial blood on measured glucose values compared with venous blood. METHODS: Forty adult patients who underwent surgery with general anesthesia were included in this study. Each patient had a cannula inserted into the radial artery and a central venous catheter through the right internal jugular vein. Two hours after the induction of anesthesia, we drew arterial and venous blood and measured the blood glucose concentration using both a bedside glucometer based on a glucose oxidase method and a laboratory glucometer based on a hexokinase method. We also measured blood gas, electrolyte, and hematocrit values. Statistical analyses were performed with repeated measure ANOVA, multiple linear regression, and Bland-Altman's analysis. Data is expressed as mean +/- SD. RESULTS: The arterial blood glucose concentration measured by the glucose oxidase method (119.5 +/- 25.0 mg/dl) was significantly lower than the venous blood (133.5 +/- 24.8 mg/dl) and hexokinase method (134.2 +/- 27.1 mg/dl). There was no significant difference between the venous blood glucose concentration by the glucose oxidase method and hexokinase method. When we used the correction formula: corrected glucose value = arterial glucose value by glucose oxidase method + 0.1053 X PaO2 - 5.414, the bias improved from - 14.6 mg/dl to 1.0 mg/dl. CONCLUSIONS: The blood glucose concentration measured by the glucose oxidase method is more accurate in venous blood than oxygenated arterial blood. When we measure the blood glucose level using the glucose oxidase method, we should consider the influence of high oxygen tension.
Adult ; Anesthesia ; Anesthesia, General ; Bias (Epidemiology) ; Blood Glucose* ; Catheters ; Central Venous Catheters ; Glucose Oxidase* ; Glucose* ; Hematocrit ; Hexokinase ; Humans ; Jugular Veins ; Linear Models ; Operating Rooms ; Oxygen* ; Radial Artery