24 research outputs found

    Peningkatan Kemampuan Pemecahan Masalah Matematis Melalui Pendekatan Matematika Realistik

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    Tujuan penelitian ini adalah untuk mendeskripsikan apakah pembelajaran matematika dengan pendekatan matematika realistis dapat meningkatkan kemampuan pemecahan masalah matematis siswa. Subjek penelitian ini adalah siswa kelas 7 dari dua SMP dengan kategori sedang yang dipilih secara acak dengan teknik purposive sampling dari seluruh SMP di Bekasi. Penelitian ini adalah penelitian eksperimen dengan desain kelompok kontrol pretes-postes. Pada kelas eksperimen dilaksanakan pembelajaran dengan pendekatan matematika realistis dan di kelompok kontrol dilaksanakan pembelajaran konvensional. Instrumen penelitian ini adalah (1) tes kemampuan pemecahan masalah matematis; (2) lembar observasi; (3) angket respon siswa; dan (4) pedoman waawancara. Analisis data dengan uji-t dan ANOVA. Hasil penelitian menunjukkan bahwa kemampuan pemecahan masalah matematis siswa yang mengikuti pembelajaran dengan pendekatan matematika realistis lebih baik daripada siswa yang mengikuti pembelajaran konvensional secara keseluruhan maupun berdasarkan kategori kemampuan matematis siswa (tinggi, sedang, rendah). Siswa dengan kemampuan matematika umum tinggi mengalami peningkatan kemampuan pemecahan masalah matematis yang lebih baik daripada siswa dengan kemampuan matematika umum sedang maupun rendah

    Predictive power of selective variables for composite endpoint of 30-day morbidity according to logistic regression analysis.

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    <p>Predictive power of selective variables for composite endpoint of 30-day morbidity according to logistic regression analysis.</p

    Skin perfusion pressure as an indicator of tissue perfusion in valvular heart surgery: Preliminary results from a prospective, observational study

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    <div><p>Hemodynamic management aims to provide adequate tissue perfusion, which is often altered during cardiac surgery with cardiopulmonary bypass (CPB). We evaluated whether skin perfusion pressure (SPP) can be used for monitoring of adequacy of tissue perfusion in patients undergoing valvular heart surgery. Seventy-two patients undergoing valve replacement were enrolled. SPP and serum lactate level were assessed after anaesthesia induction (baseline), during CPB, after CPB-off, end of surgery, arrival at intensive care unit, and postoperative 6 h. Lactate was further measured until postoperative 48 h. Association of SPP with lactate and 30-day morbidity comprising myocardial infarction, acute kidney injury, stroke, prolonged intubation, sternal infection, reoperation, and mortality was assessed. Among the lactate levels, postoperative 6 h peak value was most closely linked to composite of 30-day morbidity. The SPP value during CPB and its % change from the baseline value were significantly associated with the postoperative 6 h peak lactate (r = -0.26, P = 0.030 and r = 0.47, P = 0.001, respectively). Optimal cut-off of % decrease in SPP during CPB from baseline value for the postoperative 6 h hyperlactatemia was 48% (area under curve, 0.808; 95% confidence interval (CI), 0.652–0.963; P = 0.001). Decrease in SPP >48% during CPB from baseline value was associated with a 12.8-fold increased risk of composite endpoint of 30-day morbidity (95% CI, 1.48–111.42; P = 0.021) on multivariate logistic regression. Large decrease in SPP during CPB predicts postoperative 6 h hyperlactatemia and 30-day morbidity, which implicates a promising role of SPP monitoring in the achievement of optimal perfusion during CPB.</p></div

    Combined receiver operating characteristic curve of the % change of SPP during CPB for the postoperative 6 h hyperlactatemia (peak lactate > 3mmol/L).

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    <p>An area of 0.808 (95% confidence interval of 0.652–0.963, P = 0.001) was observed below the line of % change in SPP value. The optimal cutoff value for postoperative 6 h hyperlactatemia was 48% decrease from the baseline SPP (after induction of anesthesia), with a sensitivity and specificity of 84.6% and 77.8%, respectively. SPP = skin perfusion pressure; CPB = cardiopulmonary bypass.</p

    Effect of pregabalin administration upon reperfusion in a rat model of hyperglycemic stroke: Mechanistic insights associated with high-mobility group box 1

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    <div><p>Hyperglycemia, which reduces the efficacy of treatments and worsens clinical outcomes, is common in stroke. Ability of pregabalin to reduce neuroexcitotoxicity may provide protection against stroke, even under hyperglycemia. We investigated its protective effect against hyperglycemic stroke and its possible molecular mechanisms. Male Wistar rats administered dextrose to cause hyperglycemia, underwent middle cerebral artery occlusion for 1 h and subsequent reperfusion. Rats were treated with an intraperitoneal injection of 30 mg/kg pregabalin or an equal amount of normal saline at the onset of reperfusion (n = 16 per group). At 24 h after reperfusion, neurological deficit, infarct volume, and apoptotic cell count were assessed. Western blot analysis was performed to determine protein expression of high-mobility group box 1 (HMGB1), toll-like receptor-4 (TLR-4), phosphorylated nuclear factor-kappa B (p-NF-κB), interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), phosphorylated inducible and endothelial nitric oxide synthase (p-iNOS, p-eNOS), Bcl-2, Bax, Cytochrome C, and caspase-3 in the brain. Pregabalin-treated rats showed significantly improved neurological function (31% decrease in score), reduced infarct size (by 33%), fewer apoptotic cells (by 63%), and lower expression levels of HMGB1, TLR4, p-NF-κB, IL-1β, and TNF- α, compared with control rats. Decreased p-iNOS and increased p-eNOS expressions were also observed. Expression of Bax, Cytochrome C, and cleaved caspase-3/caspase3 was significantly downregulated, while Bcl-2 expression was increased by pregabalin treatment. Pregabalin administration upon reperfusion decreased neuronal death and improved neurological function in hyperglycemic stroke rats. Cogent mechanisms would include attenuation of HMGB1/TLR-4-mediated inflammation and favorable modulation of the NOS.</p></div
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