Benefits of an Online Interactive Educational Program Over Traditional Textbooks.

BACKGROUND: Technology has become increasingly prominent in nursing education. Online learning platforms may be more useful than traditional textbooks in promoting active learning, engagement, and satisfaction. PURPOSE: The purpose was to evaluate a new online interactive education program (OIEP) that replaces traditional textbooks and to understand student and faculty satisfaction, perceived efficacy of the program, student engagement, and whether the OIEP can help NCLEX preparation and reduce burnout. METHOD: This retrospective study assessed student and faculty perceptions of the constructs using quantitative and qualitative measures. Perceptions were measured at 2 time points each: halfway through the semester and again at its conclusion. RESULTS: Mean efficacy scores of groups were high at both time points. Students showed significant increases in content constructs, which were supported by faculty perceptions of students. Students agreed that using the OIEP throughout their program would significantly increase preparedness for NCLEX. CONCLUSION: The OIEP may better support nursing students throughout school and on NCLEX than traditional textbooks.

Assisting Learners to Understand and Incorporate Functions of Clinical Judgment Into Nursing Practice.

BACKGROUND: Mastering clinical judgment (CJ) skills is an essential competency for nurses in all health care environments. PROBLEM: Complexities of the health environment combined with the intricacies of nursing practice can pose potential risks to client safety. APPROACH: Over a 2-year period, a 3-phased approach using (1) survey results from nurses in education and practice, (2) discussion forums, and (3) a series of think tanks that comprised nurse educators resulted in the development of the Guide for CJ. OUTCOMES: The Guide for CJ provides nurse educators with an evidence-based resource to promote CJ skills in nursing students. The environmental and individual factors and expected nurse responses and behaviors contained in the Guide are well-aligned with the cognitive operations contained in the National Council of State Boards of Nursing Action Model. CONCLUSIONS: Educators may use the Guide to support faculty development and operationalize CJ to develop a variety of learning strategies for use in multiple learning environments.

Metabolic dysregulation in the SHROB rat reflects abnormal expression of transcription factors and enzymes that regulate carbohydrate metabolism.

The Koletsky (SHROB) strain of rats is spontaneously hypertensive and displays insulin resistance, hyperglucagonemia and hypertriglyceridemia but is normoglycemic under fasting conditions. The aim of this study was to unravel the pattern of expression of genes encoding key regulatory enzymes involved in carbohydrate metabolism in the liver and kidney that may be impacted in this strain. We found that SHROB animals have decreased beta-adrenergic receptor density and, consequently, blunted increases in cAMP levels in response to beta-adrenergic agonists. They also have lower levels of hepatic as well as renal phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) mRNA and protein than their lean littermates. Expression of the genes for glycogen phosphorylase and glycogen synthase was also decreased. Hepatocytes from the SHROB animals exhibited glycogen depletion of only 50% compared to 86% by hepatocytes from lean littermates when challenged with either glucagon or forskolin to stimulate adenylyl cyclase. The expression of C/EBPalpha and C/EBPbeta, two key transcription factors that are essential for the coordinated expression of genes involved in glucose homeostasis, was depressed in livers of the SHROB rats, as were levels of HNF-4alpha, PPARalpha and PGC-1alpha. We conclude that overproduction of glucose is prevented in the SHROB rats by decreased expression of the genes for glycogen phosphorylase and the gluconeogenic enzymes PEPCK and G6Pase, which may prevent progression to diabetes in this model.

Therapeutic actions of allylmercaptocaptopril and captopril in a rat model of metabolic syndrome.

BACKGROUND: Hypertension often coexists with hyperlipidemia, insulin resistance, and glucose intolerance in metabolic syndrome. Allylmercaptocaptopril is a conjugate of the angiotensin-converting enzyme inhibitor captopril with allicin, an active principle in garlic with multiple beneficial actions on metabolic-syndrome abnormalities. We sought to test the hypothesis that the conjugation of allicin to captopril may confer additional therapeutic actions in metabolic disease. METHODS: We compared allylmercaptocaptopril (53.5 mg/kg/day orally for 60 days) to an equimolar dose of captopril (40 mg/kg/day) in the spontaneously hypertensive, obese rat (SHROB) model. RESULTS: Allylmercaptocaptopril prevented progressive weight gain, without a detectable effect on food intake. Both captopril and allylmercaptocaptopril lowered blood pressure, but allylmercaptocaptopril was more effective. Allylmercaptocaptopril, but not captopril, improved cardiac hypertrophy, as indicated by heart weight and ventricular-wall thickness. Allylmercaptocaptopril improved, whereas captopril impaired, oral glucose tolerance after a fast. Triglycerides were decreased by both captopril and allylmercaptocaptopril. Total cholesterol and non-HDL cholesterol were reduced by captopril but not by allylmercaptocaptopril. The SHROB rats developed severe glomerulosclerosis and renal failure. Allylmercaptocaptopril showed significant nephro-protection, as indicated by reductions in urinary protein loss, urinary protein-to-creatinine ratio, and plasma creatinine. Captopril showed the same trends and also prevented the decline of creatinine clearance. Finally, both allylmercaptocaptopril and captopril reduced the basal level of lipolysis in isolated abdominal adipocytes, and restored the response to catecholamine stimulation. CONCLUSIONS: Both captopril and allylmercaptocaptopril are effective in attenuating multiple abnormalities of metabolic syndrome. Allylmercaptocaptopril may have additional effectiveness on improving glucose tolerance, further lowering blood pressure, reducing cardiac hypertrophy, preventing weight gain, and protecting against renal disease.

High fructose diet increases mortality in hypertensive rats compared to a complex carbohydrate or high fat diet.

BACKGROUND: Chronic hypertension leads to cardiac hypertrophy, heart failure, and premature death. Little is known about the impact of dietary macronutrient composition on hypertension-induced cardiac hypertrophy and mortality. We investigated the effects of consuming either a high complex carbohydrate diet, a high simple sugar diet, or a high fat diet on cardiac hypertrophy and mortality in hypertensive Dahl salt-sensitive (DSS) rats. METHODS: Rats were assigned to four diets: complex carbohydrate (CC; 70% starch, 10% fat, 20% protein by energy), high fat (FAT; 20% carbohydrates, 60% fat, 20% protein), high fructose (FRU; 70% fructose, 10% fat, 20% protein), and "western" (WES; 35% fructose, 45% fat, 20% protein). Hypertension was initiated by adding 6% NaCl (+S) to the chow of half the animals within each diet (n = 10 to 13/group). Tail cuff blood pressure measurements were assessed after 5 and 11 weeks of treatment, and echocardiography were assessed after 12 weeks of treatment. RESULTS: All rats fed a high salt diet had similar levels of hypertension (CC+S 220 +/-2 mm Hg, FAT+S 221 +/- 3 mm Hg, FRU+S 221 +/- 1 mm Hg, WES+S 226 +/- 3 mm Hg). Echocardiography results show that the addition of salt to FRU resulted in increased regional wall thickness that was not observed in other dietary groups. All rats fed a low salt diet (CC, FAT, FRU, WES) and the FAT+S group survived 90 days. On the other hand, there was 90-day mortality in the WES+S group (18% mortality) and the CC+S group (30% mortality). In addition, FRU+S rats started dying after 45 days of salt feeding, and only 15% survived the full 90 days. CONCLUSIONS: These results demonstrate that a high fructose diet consumed during hypertension increases mortality and left ventricular (LV) wall thickness compared to either a high fat, high starch, or a "western" diet.

High-fat diet prevents cardiac hypertrophy and improves contractile function in the hypertensive dahl salt-sensitive rat.

1. The role that dietary lipid and plasma fatty acid concentration play in the development of cardiac hypertrophy in response to hypertension is not clear. 2. In the present study, we treated Dahl salt-sensitive rats with either normal chow (NC), normal chow with salt added (NC + salt) or a diet high in long-chain saturated fatty acids with added salt (HFD + salt). Cardiac function was assessed by echocardiography and left ventricular (LV) catheterization. 3. The HFD + salt group had significantly higher plasma free fatty acid concentrations and myocardial triglyceride content compared with the NC + salt group, but did not upregulate the activity of the fatty acid oxidation enzyme medium chain acyl-coenzyme A dehydrogenase. Systolic blood pressure was elevated to a similar extent in the NC + salt and HFD + salt groups compared with the NC group. Although LV mass was increased in the NC + salt group compared with the NC group, LV mass in the HFD + salt group did not differ from that of the NC group and was significantly lower than that in the NC + salt group. 4. There was no evidence of cardiac dysfunction in the NC + salt group compared with the NC group; however, high fat feeding significantly increased LV contractile performance (e.g. increased cardiac output and peak dP/dt). 5. In conclusion, the HFD + salt diet prevented the hypertrophic response to hypertension and improved the contractile performance of the heart. It remains to be determined whether preventing cardiac hypertrophic adaptations would be deleterious to the heart if the hypertensive stress is maintained long term.

Role of C-terminal cytoplasmic domain of the AT2 receptor in ligand binding and signaling.

A stop codon at position 322 was introduced to generate a truncated, C-terminal-deleted AT2 receptor. Expression studies in Xenopus oocytes showed that C-terminal-deleted AT2 had reduced affinity to [(125)I]angiotensin II (K(d)=1.7 nM) and enhanced binding of the AT2-specific peptidic ligand [(125)I]CGP42112A (K(d)=0.097 nM). AT2 activation by angiotensin II resulted in reduction of cGMP levels in oocytes and this reduction was further enhanced by C-terminal deletion, implying that the C-terminus may have a negative effect on the AT2-mediated cGMP reduction. Moreover, interaction of the AT2 with the ATP-binding domain of the human ErbB3 receptor in yeast two-hybrid assay was abolished by C-terminal deletion. In summary, the C-terminal cytoplasmic tail of AT2 modulates its ligand binding and signaling properties.