This article is being retracted as a part of the manuscript was a 'duplicate publication' from an earlier publication.

No abstract available.
Delivery of Health Care* ; Family Practice* ; Humans

No abstract available.
Delivery of Health Care* ; Family Practice* ; Humans

No abstract available.
Histiocytoma, Benign Fibrous*

No abstract available.
Urinary Tract Infections* ; Urinary Tract*

BACKGROUND: Oxidative stress occurs in white adipose tissue and dysregulates the expression of adipokines secreted from adipocytes. Since adipokines influence inflammation, supplementation with antioxidants might be beneficial for preventing oxidative stress-mediated inflammation in adipocytes and inflammation-associated complications. β-Carotene is the most prominent antioxidant carotenoid and scavenges reactive oxygen species in various tissues. The purpose of this study was to determine whether β-carotene regulates the expression of adipokines, such as adiponectin, monocyte chemoattractant protein-1 (MCP-1), and regulated on activation, normal T cell expressed and secreted (RANTES) in 3T3-L1 adipocytes treated with glucose/glucose oxidase (G/GO). METHODS: 3T3-L1 adipocytes were cultured with or without β-carotene and treated with G/GO, which produces H2O2. mRNA and protein levels in the medium were determined by a real-time PCR and an ELISA. DNA binding activities of transcription factors were assessed using an electrophoretic mobility shift assay. RESULTS: G/GO treatment increased DNA binding affinities of redox-sensitive transcription factors, such as NF-κB, activator protein-1 (AP-1), and STAT3. G/GO treatment reduced the expression of adiponectin and increased the expression of MCP-1 and RANTES. G/GO-induced activations of NF-κB, AP-1, and STAT3 were inhibited by β-carotene. G/GO-induced dysregulation of adiponectin, MCP-1, and RANTES were significantly recovered by treatment with β-carotene. CONCLUSIONS: β-Carotene inhibits oxidative stress-induced inflammation by suppressing pro-inflammatory adipokines MCP-1 and RANTES, and by enhancing adiponectin in adipocytes. β-Carotene may be beneficial for preventing oxidative stress-mediated inflammation, which is related to adipokine dysfunction.
Adipocytes ; Adipokines ; Adiponectin ; Adipose Tissue, White ; Antioxidants ; beta Carotene ; Chemokine CCL2 ; Chemokine CCL5 ; DNA ; Electrophoretic Mobility Shift Assay ; Enzyme-Linked Immunosorbent Assay ; Inflammation ; Oxidative Stress ; Oxidoreductases ; Reactive Oxygen Species ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; Transcription Factor AP-1 ; Transcription Factors

PURPOSE: The purpose of this study was to identify the features, risk scores and risk factors for deep vein thrombosis in critically ill patients who developed deep vein thrombosis in their lower extremities. METHODS: The participants in this prospective descriptive study were 175 adult patients who did not receive any prophylactic medication or mechanical therapy during their admission in the intensive care unit. RESULTS: The mean age was 62.24 (+/-17.28) years. Men made up 54.9% of the participating patients. There were significant differences in age, body mass index, and leg swelling between patients who developed deep vein thrombosis and those who did not have deep vein thrombosis. The mean risk score was 6.71(+/-2.94) and they had on average 4.01(+/-1.35) risk factors. In the multiple logistic regression, body mass index (odds ratio=1.14) and leg swelling (odds ratio=6.05) were significant predictors of deep vein thrombosis. CONCLUSION: Most critically ill patients are in the potentially high risk group for deep vein thrombosis. However, patients who are elderly, obese or have leg edema should be closely assessed and more than one type of active prophylactic intervention should be provided.
Adolescent ; Adult ; Age Factors ; Aged ; Aged, 80 and over ; Body Mass Index ; *Critical Illness ; Female ; Humans ; Leg/*blood supply ; Logistic Models ; Male ; Middle Aged ; Odds Ratio ; Predictive Value of Tests ; Prospective Studies ; Risk Factors ; Venous Thrombosis/diagnosis/*etiology ; Young Adult

OBJECTIVES: The purpose of this descriptive study was to investigate the current situation of clinical alarms in intensive care unit (ICU), nurses' recognition of and fatigue in relation to clinical alarms, and obstacles in alarm management. METHODS: Subjects were ICU nurses and devices from 48 critically ill patient cases. Data were collected through direct observation of alarm occurrence and questionnaires that were completed by the ICU nurses. The observation time unit was one hour block. One bed out of 56 ICU beds was randomly assigned to each observation time unit. RESULTS: Overall 2,184 clinical alarms were counted for 48 hours of observation, and 45.5 clinical alarms occurred per hour per subject. Of these, 1,394 alarms (63.8%) were categorized as false alarms. The alarm fatigue score was 24.3 +/- 4.0 out of 35. The highest scoring item was "always get bothered due to clinical alarms". The highest scoring item in obstacles was "frequent false alarms, which lead to reduced attention or response to alarms". CONCLUSIONS: Nurses reported that they felt some fatigue due to clinical alarms, and false alarms were also obstacles to proper management. An appropriate hospital policy should be developed to reduce false alarms and nurses' alarm fatigue.
Clinical Alarms* ; Critical Care* ; Critical Illness ; Fatigue* ; Humans ; Intensive Care Units*

BACKGROUND: Midazolam relaxes airway smooth muscle. The aim of this study is to evaluate the influence of flumazenil or verapamil on the relaxation effects of midazolam in tracheal smooth muscle of guinea pig. METHODS: After isolating guinea-pig tracheal preparations, the maximal tracheal tones were induced by 2 10(-7) M carbachol. When tracheal tones stabilized, midazolam was added cumulatively (10(-6), 3 10(-6), 10(-5), 3 10(-5), 10(-4) M, n=14) with or without flumazenil (10(-6) M, n=15) and verapamil (10(-5) M, n=13) to obtain the concentration-relaxation curves, and then the ED50 and ED95 calculated. RESULTS: Midazolam decreased maximal tracheal smooth muscle tones in concentration-dependent manners. Pretreatment with flumazenil had no effect on the midazolam-induced relaxation. Verapamil enhanced the relaxation effect of midazolam. CONCLUSIONS: Midazolam relaxes airway smooth muscle and has synergistic effect with calcium channel blocker, verapamil.
Animals ; Calcium Channels ; Carbachol ; Flumazenil* ; Guinea Pigs ; Midazolam* ; Muscle, Smooth* ; Relaxation* ; Verapamil*

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.
Acetylcholine ; Action Potentials ; Adenosine ; Animals ; Atropine ; Carbachol ; Cholinergic Agonists* ; Hand ; Ischemia ; Microelectrodes ; Myocardium* ; Rats*