Differential effects of mTOR inhibition and dietary ketosis in a mouse model of subacute necrotizing encephalomyelopathy.

Genetic mitochondrial diseases are the most frequent cause of inherited metabolic disorders and one of the most prevalent causes of heritable neurological disease. Leigh syndrome is the most common clinical presentation of pediatric mitochondrial disease, typically appearing in the first few years of life, and involving severe multisystem pathologies. Clinical care for Leigh syndrome patients is difficult, complicated by the wide range of symptoms including characteristic progressive CNS lesion, metabolic sequelae, and epileptic seizures, which can be intractable to standard management. While no proven therapies yet exist for the underlying mitochondrial disease, a ketogenic diet has led to some reports of success in managing mitochondrial epilepsies, with ketosis reducing seizure risk and severity. The impact of ketosis on other aspects of disease progression in Leigh syndrome has not been studied, however, and a rigorous study of the impact of ketosis on seizures in mitochondrial disease is lacking. Conversely, preclinical efforts have identified the intracellular nutrient signaling regulator mTOR as a promising therapeutic target, with data suggesting the benefits are mediated by metabolic changes. mTOR inhibition alleviates epilepsies arising from defects in TSC, an mTOR regulator, but the therapeutic potential of mTOR inhibition in seizures related to primary mitochondrial dysfunction is unknown. Given that ketogenic diet is used clinically in the setting of mitochondrial disease, and mTOR inhibition is in clinical trials for intractable pediatric epilepsies of diverse causal origins, a direct experimental assessment of their effects is imperative. Here, we define the impact of dietary ketosis on survival and CNS disease in the Ndufs4(KO) mouse model of Leigh syndrome and the therapeutic potential of both dietary ketosis and mTOR inhibition on seizures in this model. These data provide timely insight into two important clinical interventions.

Regional metabolic signatures in the Ndufs4(KO) mouse brain implicate defective glutamate/α-ketoglutarate metabolism in mitochondrial disease.

Leigh Syndrome (LS) is a mitochondrial disorder defined by progressive focal neurodegenerative lesions in specific regions of the brain. Defects in NDUFS4, a subunit of complex I of the mitochondrial electron transport chain, cause LS in humans; the Ndufs4 knockout mouse (Ndufs4(KO)) closely resembles the human disease. Here, we probed brain region-specific molecular signatures in pre-symptomatic Ndufs4(KO) to identify factors which underlie focal neurodegeneration. Metabolomics revealed that free amino acid concentrations are broadly different by region, and glucose metabolites are increased in a manner dependent on both region and genotype. We then tested the impact of the mTOR inhibitor rapamycin, which dramatically attenuates LS in Ndufs4(KO), on region specific metabolism. Our data revealed that loss of Ndufs4 drives pathogenic changes to CNS glutamine/glutamate/α-ketoglutarate metabolism which are rescued by mTOR inhibition Finally, restriction of the Ndufs4 deletion to pre-synaptic glutamatergic neurons recapitulated the whole-body knockout. Together, our findings are consistent with mTOR inhibition alleviating disease by increasing availability of α-ketoglutarate, which is both an efficient mitochondrial complex I substrate in Ndufs4(KO) and an important metabolite related to neurotransmitter metabolism in glutamatergic neurons.

Comparative effectiveness of different antiplatelet agents at reducing TNF-driven inflammatory responses in a mouse model.

Antiplatelet drugs are conventionally used as treatments because of their anti-coagulation functions. However, their pleiotropic effects are of great significance to the treatment of ischaemic cardiovascular diseases. Many studies have reported that an excessive amount of inflammation driven by tumour necrosis factor (TNF) is closely related to the prevalence of atherosclerosis. As the drug selection criteria and evaluation methods related to the anti-TNF activity of antiplatelet drugs remain limited, our investigation of these drugs should prove beneficial. In this study, we compared the anti-TNF activity of three antiplatelet agents, namely clopidogrel, sarpogrelate, and cilostazol, using the TNF-induced inflammatory mouse model. After the oral administration of these drugs, acute inflammation was induced via injection of lipopolysaccharide (LPS) or D-galactosamine (D-gal) and TNF. Serum TNF levels, and the mRNA and protein expression levels of TNF in mouse heart tissue, macrophage accumulation in aortic lesions, and mouse survival were analysed to compare the anti-TNF effects of the three antiplatelet agents. Of the three antiplatelet agents, cilostazol significantly reduced the different levels under the most effective observation. In addition, cilostazol was found to attenuate the TNF-stimulated phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) p65 in the aortic vascular smooth muscle cell line, MOVAS-1 and the D-gal plus TNF-challenged heart tissue of mouse. Therefore, cilostazol is the most ideal of the three antiplatelet drugs for the treatment of TNF-mediated inflammatory disorders.

A Comparison of the Anti-Inflammatory Effects of Four Combined Statin and Antiplatelet Therapies on Tumor Necrosis Factor-Mediated Acute Inflammation in vivo.

BACKGROUND: Combination therapy has been administered to patients with chronic or complex diseases due to its improved therapeutic effects compared with the results of monotherapy. Due to the pleiotropic effects of statins and antiplatelets, these drugs have been studied in combination with other drugs, but not all combinations exerted obvious beneficial effects compared with individual drugs. In this study, we aimed to compare the anti-inflammatory effects of 4 different combination therapies of statins and antiplatelets on the tumor necrosis factor (TNF)-mediated inflammation in vivo. METHODS: Mice were orally administered cilostazol plus pravastatin (CILOP) or cilostazol plus rosuvastatin (CILOR), clopidogrel plus pravastatin (CLOP), or clopidogrel plus rosuvastatin (CLOR); then, acute inflammation was induced by the injection of lipopolysaccharide (LPS) or TNF. Serum TNF levels, macrophage accumulation in the lesioned aortas, and mouse mortality were observed to be comparable to the anti-inflammatory effects of the combination therapies. RESULTS: In mice with LPS-induced inflammation, CILOP and CILOR substantially reduced macrophage infiltration of aortic lesions and the serum TNF levels compared with CLOP and CLOR. Moreover, among the 4 combinations, CILOP significantly improved the survival rate of mice with TNF-mediated acute lethal inflammation. CONCLUSIONS: The combination therapy comprising cilostazol and statins, particularly pravastatin, exerted the best anti-TNF effect compared with clopidogrel and statin therapy; thus, a suitable combination therapy, such as CILOP, can be a potential remedy to cure TNF-related diseases.

Anti-TNF effect of combined pravastatin and cilostazol treatment in an in vivo mouse model.

Objectives: Pravastatin and cilostazol are used as lipid-lowering and antiplatelet agents, respectively. Regarding their well-known anti-inflammatory effects, the additive effect of the two drugs on anti-TNF functions has not yet been investigated. In the present investigation, the beneficial effect of combined pravastatin and cilostazol on their anti-TNF activities was assessed using an in vivo mouse model. Methods: Mice were pretreated with pravastatin and/or cilostazol (40 mg/kg of each), orally once two hour prior to an LPS (5 mg/kg, i.p.) challenge. One hour post challenge, blood and descending aorta were collected for serum TNF levels and immune cell infiltration analyses. For survival analysis, pravastatin and/or cilostazol (40 mg/kg of each) were administered 30 minutes prior to d-galactosamine administration (700 mg/kg, i.p.) and TNF (10 µg/kg, i.p.) challenge and mice survival was monitored. We also examined the effect of either drug or the combination of drugs on TNF-mediated MAPK and NF-κB signaling, using Western blot analysis. Results: Combined treatment of pravastatin and cilostazol significantly decreased serum TNF release and immune cell infiltration in the descending aorta following LPS administration, compared to each single treatment. Additionally, the combined drugs significantly decreased TNF-mediated mouse mortality and downregulated TNF-induced MAPK and NF-κB activation. Conclusions: These findings suggest that combined pravastatin and cilostazol is more effective for reducing TNF-driven inflammation through their anti-TNF activity than monotherapy.

A Novel Small-Molecule Inhibitor Targeting the IL-6 Receptor ß Subunit, Glycoprotein 130.

IL-6 is a major causative factor of inflammatory disease. Although IL-6 and its signaling pathways are promising targets, orally available small-molecule drugs specific for IL-6 have not been developed. To discover IL-6 antagonists, we screened our in-house chemical library and identified LMT-28, a novel synthetic compound, as a candidate IL-6 blocker. The activity, mechanism of action, and direct molecular target of LMT-28 were investigated. A reporter gene assay showed that LMT-28 suppressed activation of STAT3 induced by IL-6, but not activation induced by leukemia inhibitory factor. In addition, LMT-28 downregulated IL-6-stimulated phosphorylation of STAT3, gp130, and JAK2 protein and substantially inhibited IL-6-dependent TF-1 cell proliferation. LMT-28 antagonized IL-6-induced TNF-α production in vivo. In pathologic models, oral administration of LMT-28 alleviated collagen-induced arthritis and acute pancreatitis in mice. Based on the observation of upstream IL-6 signal inhibition by LMT-28, we hypothesized IL-6, IL-6Rα, or gp130 to be putative molecular targets. We subsequently demonstrated direct interaction of LMT-28 with gp130 and specific reduction of IL-6/IL-6Rα complex binding to gp130 in the presence of LMT-28, which was measured by surface plasmon resonance analysis. Taken together, our data suggest that LMT-28 is a novel synthetic IL-6 inhibitor that functions through direct binding to gp130.

Factors influencing the confidence in core clinical skills among hospital nurses.

The purpose of this study was to examine the confidence to perform 20 clinical skills and identify factors influencing the confidence of hospital nurses. A descriptive, cross-sectional study was conducted with 550 hospital nurses at four hospitals in B city, Korea. The confidence to perform, frequency of performance and educational needs on 20 clinical skills identified by Korean Accreditation Board of Nursing were measured with a self-reported questionnaire. Data were analysed by SPSS 19.0 (IBM Corporation, Armonk, New York, USA). Participants were 27 years old on average, and 49.5% had less than 3 years of total working experience. The most confident skill was measuring vital signs, whereas the least confident skill was using defibrillator. In results of stepwise regression, confidence to perform was associated with educational needs, total working experience, frequency of performance and position. It is necessary to give opportunities to practice clinical skills at both schools and clinics for producing well-prepared nurses.

Leukocytes mediate disease pathogenesis in the Ndufs4(KO) mouse model of Leigh syndrome.

Symmetric, progressive, necrotizing lesions in the brainstem are a defining feature of Leigh syndrome (LS). A mechanistic understanding of the pathogenesis of these lesions has been elusive. Here, we report that leukocyte proliferation is causally involved in the pathogenesis of LS. Depleting leukocytes with a colony-stimulating factor 1 receptor inhibitor disrupted disease progression, including suppression of CNS lesion formation and a substantial extension of survival. Leukocyte depletion rescued diverse symptoms, including seizures, respiratory center function, hyperlactemia, and neurologic sequelae. These data reveal a mechanistic explanation for the beneficial effects of mTOR inhibition. More importantly, these findings dramatically alter our understanding of the pathogenesis of LS, demonstrating that immune involvement is causal in disease. This work has important implications for the mechanisms of mitochondrial disease and may lead to novel therapeutic strategies.

Mechanisms underlying neonate-specific metabolic effects of volatile anesthetics.

Volatile anesthetics (VAs) are widely used in medicine, but the mechanisms underlying their effects remain ill-defined. Though routine anesthesia is safe in healthy individuals, instances of sensitivity are well documented, and there has been significant concern regarding the impact of VAs on neonatal brain development. Evidence indicates that VAs have multiple targets, with anesthetic and non-anesthetic effects mediated by neuroreceptors, ion channels, and the mitochondrial electron transport chain. Here, we characterize an unexpected metabolic effect of VAs in neonatal mice. Neonatal blood ß-hydroxybutarate (ß-HB) is rapidly depleted by VAs at concentrations well below those necessary for anesthesia. ß-HB in adults, including animals in dietary ketosis, is unaffected. Depletion of ß-HB is mediated by citrate accumulation, malonyl-CoA production by acetyl-CoA carboxylase, and inhibition of fatty acid oxidation. Adults show similar significant changes to citrate and malonyl-CoA, but are insensitive to malonyl-CoA, displaying reduced metabolic flexibility compared to younger animals.

Beneficial anti-inflammatory effects of combined rosuvastatin and cilostazol in a TNF-driven inflammatory model.

BACKGROUND: Due to anti-inflammatory and anti-thrombotic functions, statins and antiplatelets are widely used for patients with cardiovascular-related or coronary artery diseases. Patients with systemic or complex diseases are commonly prescribed multiple targeted medications; thus, a proper combination of two or more drugs for beneficial efficacy is considered in clinical therapy. Recent studies have suggested that combinational therapy with statins and other medications accelerates their single effect to suppress inflammatory responses. However, the therapeutic efficacy and underlying mechanism of combination treatment with rosuvastatin and cilostazol have been poorly studied. METHODS: Mice were administered rosuvastatin alone, cilostazol alone or rosuvastatin and cilostazol in combination, and then injected with LPS or TNF to induce acute inflammation. The serum TNF level, macrophage infiltration of the lesioned aortas and mice mortality were observed in the acute inflammation model. The phosphorylation of MAPK was analyzed in TNF-stimulated HeLa cells. RESULTS: Compared to the treatment with cilostazol alone, the combination treatment with rosuvastatin and cilostazol significantly reduced not only the levels of TNF in the sera but also macrophage infiltration in aortic lesions. In addition, the combination therapy decreased TNF-mediated phosphorylation of the MAPK signaling pathway and improved the survival rate in the TNF-driven inflammatory mice model. CONCLUSION: Rosuvastatin combined with cilostazol therapy can greatly improve the anti-inflammatory effect of monotherapies, resulting in reduced mortality of mice; thus, we propose the potential of use of this combination therapy as anti-TNF agent.

Combination therapy with cilostazol and pravastatin improves antiatherogenic effects in low-density lipoprotein receptor knockout mice.

AIMS: Despite the therapeutic efficacy of statins and antiplatelet agents for atherosclerosis, monotherapy with each drug alone is often insufficient to achieve the patient's therapeutic goals. We previously showed that combined statin/antiplatelet agent/anti-tumor necrosis factor (TNF) agent therapy (pravastatin/sarpogrelate/etanercept) reduces atherosclerotic lesions by inhibiting TNF, an atherogenic cytokine that contributes to the progression of arteriosclerosis. In addition, our previous study showed that combined treatment with pravastatin and cilostazol is effective for reducing TNF-driven inflammation through anti-TNF activity. Therefore, in the present study, we evaluated the additive effects of combined pravastatin and cilostazol therapy on atherosclerotic progression using low-density lipoprotein receptor (LDLR) knockout (KO) mice. METHODS: Ten-week-old LDLR KO mice were fed a high-fat, high-cholesterol diet and orally administered pravastatin and cilostazol alone or in combination. Body weight, plasma lipid levels, and the levels of intracellular adhesion molecules and inflammatory cytokines were analyzed. In addition, aortas and aortic roots were stained with Oil Red O, and atherosclerotic plaques were quantified. RESULTS: The atherosclerotic plaques in the combined pravastatin and cilostazol treatment groups were significantly reduced compared to those in each drug monotherapy group. The combination therapy group also showed the downregulation of ICAM-1, MOMA-2, TNF, interleukin (IL)-6, triglyceride, total cholesterol, and low-density lipoprotein levels and the upregulation of high-density lipoprotein levels compared to those of the pravastatin- or cilostazol-treated groups. CONCLUSIONS: Our results suggest that combination therapy with pravastatin and cilostazol exerts beneficial effects by decreasing atherosclerotic lesion progression and improving the pro-inflammatory state in the vascular endothelium. These effects are mediated by the reduction in adhesion molecule expression, immune cell infiltration, and cytokine levels and the antiatherosclerotic modulation of serum cholesterol levels. Therefore, we conclude that combined treatment with pravastatin and cilostazol may be a more effective antiatherosclerotic strategy than treatment with either agent alone.

[Risk factors for nosocomial urinary tract infection in the intensive care unit with a positive urine culture and foley catheterization].

PURPOSE: The purpose of this study was to identify the risk factors for a nosocomial urinary tract infection in intensive care units with a foley catheterization which showed a positive urine culture. METHOD: Three-hundred eighty-seven patients were included in the study. A retrospective review of the electrical medical record system's databases and medical record sheets in hospitalized patients from January 2003 to December 2003 was used. The collected data was analyzed by descriptive statistics, t-test, chi-square test and logistic regression analysis. RESULT: The frequency of the participants' nosocomial urinary tract infection was 72.9%. Significant risk factors for a nosocomial urinary tract infection were 'age', 'place of catheter insertion', 'frequency of catheter change', and 'duration of catheterization'. These variables explained 18.4% of variance in the experience of nosocomial urinary tract infection in intensive care units with foley catheterization. CONCLUSION: Medical personnel can decrease the incidence of a nosocomial urinary tract infection by recognizing and paying attention to the duration of catheterization, frequency of catheter change, and place of catheter insertion. As a result, specific and scrupulous strategies should be developed to reflect these factors for decreasing nosocomial urinary tract infections.

[Prediction of perceived health status on job stress and family stress with middle school teachers].

PURPOSE: The purpose of this study was to identify the relationship among job stress, family stress and perceived health status of middle school teachers and to present basic information about promoting health and coping with stress. METHOD: Participants(N=547) was recruited in B city from November 2005 to December 2005. Data were analyzed with descriptive statistics, t-test, ANOVA, Pearson's correlation and multiple regression. RESULTS: The degree of job stress of the middle school teachers was 54.47 out of a total score of 88; that of family stress was 46.57 out of a total score of 96; and that of perceived health status was 78.59 out of the perfect score 100. There was a significantly negative relationship between job stress and perceived health status (r=-.274, p<.001), and family stress and perceived health status(r=-.408, p<.001). However, there was a positive relationship between job stress and family stress(r=.298, p<.001). Family stress, gender, charging subject, job stress, charging grade and number of family member was 27.1% of the variance in perceived health status of middle school teachers. CONCLUSION: Family stress has the most important impact on perceived health status with middle school teachers. Based on the finding, we could conclude that both job stress and family stress management should be required to improve perceived health status.

Critical role of TNF inhibition in combination therapy for elderly mice with atherosclerosis.

AIMS: We have previously shown that the combination of pravastatin and sarpogrelate is synergistically beneficial for atherosclerosis. In this study, we investigated whether the pravastatin-sarpogrelate combination was sufficient for treatment in an old mouse model of atherosclerosis or if additional intervention would be needed to address the newly included aging factor and its complex pathophysiological impact on the atherosclerogenic state. We added an anti-TNF biological to the combination treatment cocktail because of the known pathologic roles of TNF in the aging process. METHODS: Sixty-week-old low-density lipoprotein receptor knockout mice were fed a high-fat, high-cholesterol diet and treated with the sarpogrelate and pravastatin combination, etanercept alone, or the triple combination. RESULTS: Although, etanercept alone did not significantly reduce aortic root and atherosclerotic plaque areas, the pravastatin-sarpogrelate combination, and pravastatin-sarpogrelate-etanercept triple therapy significantly reduced the plaque areas. Surprisingly, TNF inhibition was critically required to reduce the plaque areas of aortic roots and the expression of ICAM-1, MOMA-2, and TNF. More importantly, a lipid-lowering effect by pravastatin was observed only in the triple therapy group and not in the pravastatin and sarpogrelate combination group. CONCLUSIONS: These results suggest that TNF-inhibitory intervention should be added to the conventional therapy as a novel strategy for treating the elderly patients with atherosclerosis.

Comparing the Postoperative Complications, Hospitalization Days and Treatment Expenses Depending on the Administration of Postoperative Prophylactic Antibiotics to Hysterectomy.

PURPOSE: This study was conducted to compare postoperative complications, hospitalization days and treatment expenses to postoperative prophylactic antibiotics administrated to hysterectomy or not. METHODS: A retrospective survey study was performed with 128 cases in which elective hysterectomy had undergone. They were divided into two groups by identifying whether postoperative prophylactic antibiotics was administered for hysterectomy: a) one group who received postoperative prophylactic antibiotics and; b) those who did not. Data were collected using the electric medical record at a hospital and analyzed by SPSS 23.0 for χ2 test, t-test and ANCOVA. RESULTS: Postoperative complications including wound infection (p=1.000), pneumonia (p=.496), hematoma (p=.530), and pneumoperitoneum (p=.496) showed no significant differences between two groups. Hospitalization days for the prophylactic antibioticsadministrated group were significantly longer than the non-administered for prophylactic antibiotics (p=.004). The treatment expenses of the prophylactic antibiotics-administrated group were significantly higher than those of the non-administered prophylactic antibiotics (F=4.31, p=.040). CONCLUSION: These results can be provided for the evidence of administrating postoperative prophylactic antibiotics to hysterectomy. Additionally, it can contribute to decreasing the medication errors caused by infrequently administrating postoperative prophylactic antibiotics as well as to lessening likelihood of infection of intravenous injection site.

[The effects of a rehabilitation program on physical health, physiological indicator and quality of life in breast cancer mastectomy patients].

PURPOSE: The purpose of this study was to investigate the effects of a rehabilitation program on physical health, physiological indicators and quality of life in breast cancer mastectomy patients. METHODS: The subjects included thirty-one patients with breast cancer (17 in the experimental group and 14 in the control group). The subjects in the experimental group participated in a rehabilitation program for 10 weeks, which was composed of an exercise program, teaching, counseling and support for 2 sessions per week. RESULTS: There was a significant increase in flexion, internal rotation and external rotation but no significant increase in extension in the experimental group compared to the control group. The total cholesterol, triglyceride, HDL, LDL, and CD56 in the experimental group compared to the control group was not significantly decreased after the rehabilitation program. Compared to the control group, quality of life in the experimental group was significantly improved and fatigue in that group was significantly decreased after the rehabilitation program. CONCLUSION: The 10-week rehabilitation program showed a large affirmative effect on physical health, physiological indicators and quality of life in breast cancer mastectomy patients.

[A study on health perception and health promoting behavior in chronic back pain patients].

PURPOSE: The purpose of this study was to show a relationship between health perception and health promoting behaviors in chronic low back pain patients. METHOD: The subjects for this study were 213 persons who the visited hospital with low back pain-related problems. RESULTS: The higher the level of the health perception in chronic back pain patients was the higher the rate of the practice of health promoting behaviors (r=0.393, p<.001). The health perception T score was 50.00+/-10.00. As for health promoting behaviors, the T score was 49.99+/-10.00. The subscale of the highest mean score was interpersonal support (2.96+/-0.64) and the subscale of the lowest mean score was exercise (2.13+/-0.99). CONCLUSION: This study showed that chronic low back pain patients had a lower level of perception of their health, and their practice to improve their health was not enough. Therefore, nurses should educate and encourage chronic low back pain patients in proper exercises and correct posture to strengthen and maintain lumbar extension muscle power.

Pravastatin and Sarpogrelate Synergistically Ameliorate Atherosclerosis in LDLr-Knockout Mice.

Pravastatin is a lipid-lowering agent that attenuates atherosclerosis. However, the multifactorial pathogenesis of atherosclerosis requires other drugs with different anti-atherogenic mechanisms. We chose sarpogrelate as an anti-platelet agent and a novel component of a complex drug with pravastatin due to its high potential but little information on its beneficial effects on atherosclerosis. Low-density lipoprotein receptor-knockout mice were fed a high-fat, high-cholesterol diet and treated with pravastatin alone, sarpogrelate alone, or a combination of both drugs. Although sarpogrelate alone did not significantly reduce atherosclerotic plaque areas, co-treatment with pravastatin significantly decreased aortic lesions compared to those of the pravastatin alone treated group. The combined therapy was markedly more effective than that of the single therapies in terms of foam cell formation, smooth muscle cell proliferation, and inflammatory cytokine levels. These results suggest that pravastatin and sarpogrelate combined therapy may provide a new therapeutic strategy for treating atherosclerosis.

[Body weight, cardiovascular risk factors, and self-efficacy of diabetic control among obese type II diabetic patients].

PURPOSE: The purpose of this study was to examine the effects of problem solving nursing counseling and walking exercise on weight loss, cardiovascular risk factors, and self-efficacy of diabetic control among obese diabetic patients. The Polar heart rate monitor was used for walking exercise to utilize the Biofeedback mechanism. METHOD: Fifty nine diabetic patients were conveniently placed into experimental (n=35) and control groups (n=24). The experimental group participated in weekly nursing counseling for 12 weeks and was encouraged to do walking exercise using a Polar monitor. The control group remained in the same treatment as before. The data was collected from November 2003 to August 2004 and analyzed using t-tests and ANCOVAs. RESULTS: After 12 weeks, the participants in the experimental group reported significantly decreased body weight (p=.004) and total scores on the Parma scale (p=.001). While the participants in the control group reported significantly increased levels of blood triglyceride (p=.046) and HDL (p=.018). CONCLUSION: Based on the findings, we concluded that problem focused nursing counseling with intensified walking exercise could reduce the risk of cardiovascular complications and body weight among obese diabetic patients. Future research to explore the long-term effects of nursing counseling on diabetic complications is warranted.

[Factors influencing the development of pressure ulcers in surgical patients].

PURPOSE: The purpose of this study was to identify the influencing factors on the development of pressure ulcers in patients undergoing surgery which lasted more than two hours. METHOD: One hundred nineteen surgical adult patients were included in the study. Data was measured on each participant from December 2003 to February 2004. It was collected using a structured researcher-administered sheet and analyzed by descriptive statistics, t-test, chi-square test and logistic regression analysis. RESULT: The prevalence of a perioperative pressure ulcer was 26.1%. The level of moisture, friction and shear, length of surgery, and perioperative irrigation were significantly higher in the pressure ulcer group than those in the non-pressure ulcer group. The level of activity and level of consciousness were significantly lower in the pressure ulcer group than those in the non-pressure ulcer group. Significant influencing factors on the development of pressure ulcer were 'moisture' and 'irrigation' and those variables explained 23.1% of variance in the development of a pressure ulcer during surgery. CONCLUSION: It is necessary to develop a strategy to prevent pressure ulcer by taking 'moisture' and 'irrigation' into account during the preoperative, perioperative and postoperative period.