Pengembangan Perangkat Pembelajaran Matematika Kelas Rendah Berorientasi Model Pembelajaran Diskusi

This development was aimed at creating learning device for low level mathematics to increase the students\u27 participation and achievement through discussion learning model in Class A of the second semester of the Elementary School Teacher Education Department of Muhammadiyah University of Purwokerto of the academic year 2008/2009. The 49 subject takers was divided into 15 groups of 3 to 4 people. The procedure of developing the device used classroom action research. The action consisted of two cycles and took three months. Each cycle was done depending on the obtained improvement, design and the factor to be developed. The instrument which was used to get the data of participation and students\u27 response towards the lecture and the learning device was questioner, while he instrument to get data on students learning achievement were essay quiz, mid term test, and the end term test. The result was the device for learning low level mathematics, early-class learning material, students work, and increased learning participation. The learning achievement was still low which was due to their low ability in solving mathematical problem. Key words: Discussion learning model, participation, and mathematics learning achievement

Self-assembled lamellar-type nanostructure in manganite spinel (Co, Mn, Fe)3O4

Distinct nanostructures in (Co,Mn,Fe)3O4 were investigated using X-ray diffraction techniques combined with transmission and scanning transmission electron microscopy, as well as energy dispersive X-ray spectroscopy. The size of the checkerboard nanostructure increased with annealing, followed by the appearance of lamellar nanostructures comprising different types of platelike nanodomains because of nanoscopic spinodal decomposition of Mn and Fe ions. Remarkable local strain relaxation at the nanoscale associated with the domain size is suggested to play an important role in the stabilization of these checkerboard and lamellar nanostructures

Balancing intestinal and systemic inflammation through cell type-specific expression of the aryl hydrocarbon receptor repressor

As a sensor of polyaromatic chemicals the aryl hydrocarbon receptor (AhR) exerts an important role in immune regulation besides its requirement for xenobiotic metabolism. Transcriptional activation of AhR target genes is counterregulated by the AhR repressor (AhRR) but the exact function of the AhRR in vivo is currently unknown. We here show that the AhRR is predominantly expressed in immune cells of the skin and intestine, different from other AhR target genes. Whereas AhRR antagonizes the anti-inflammatory function of the AhR in the context of systemic endotoxin shock, AhR and AhRR act in concert to dampen intestinal inflammation. Specifically, AhRR contributes to the maintenance of colonic intraepithelial lymphocytes and prevents excessive IL- 1β production and Th17/Tc17 differentiation. In contrast, the AhRR enhances IFN-γ-production by effector T cells in the inflamed gut. Our findings highlight the physiologic importance of cell-type specific balancing of AhR/AhRR expression in response to microbial, nutritional and other environmental stimuli

Changes in Atrial Size Following PVI: Comparison of the Right and Left Atria

Background: Pulmonary vein isolation (PVI) is expected to cure atrial fibrillation (AF) and to improve atrial remodeling. However, the effects of PVI on the right atrial (RA) size have not been fully examined. We studied the effects of PVI on RA size in comparison that with the effects on LA size. Method: We studied 17 patients with drug-refractory AF (11 paroxysmal, 6 persistent). Two-dimensional echocardiography was performed at baseline and at follow-up to measure and compare RA and LA size.Results: Despite a short duration of AF in 7 patients after the PVI, all cases were maintained in sinus rhythm during the follow-up. LA and RA size were both reduced after the PVI compared with baseline measurements (LA 25.5 ± 2.9cm2 vs. 23.2 ± 3.6cm2, P < 0.05, RA 21.2 ± 2.9cm2 vs. 18.1 ± 3.0cm2, P < 0.01). The reduction ratio was more prominent in RA size (14.9%) than in LA size (8.7%)(P < 0.05). Conclusion: Atrial size was reduced following PVI for both the LA and RA, although the rate of reduction was more prominent in the RA

Autophagy Induction as a Therapeutic Strategy for Neurodegenerative Diseases.

Autophagy is a major, conserved cellular pathway by which cells deliver cytoplasmic contents to lysosomes for degradation. Genetic studies have revealed extensive links between autophagy and neurodegenerative disease, and disruptions to autophagy may contribute to pathology in some cases. Autophagy degrades many of the toxic, aggregate-prone proteins responsible for such diseases, including mutant huntingtin (mHTT), alpha-synuclein (α-syn), tau, and others, raising the possibility that autophagy upregulation may help to reduce levels of toxic protein species, and thereby alleviate disease. This review examines autophagy induction as a potential therapy in several neurodegenerative diseases-Alzheimer's disease, Parkinson's disease, polyglutamine diseases, and amyotrophic lateral sclerosis (ALS). Evidence in cells and in vivo demonstrates promising results in many disease models, in which autophagy upregulation is able to reduce the levels of toxic proteins, ameliorate signs of disease, and delay disease progression. However, the effective therapeutic use of autophagy induction requires detailed knowledge of how the disease affects the autophagy-lysosome pathway, as activating autophagy when the pathway cannot go to completion (e.g., when lysosomal degradation is impaired) may instead exacerbate disease in some cases. Investigating the interactions between autophagy and disease pathogenesis is thus a critical area for further research

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension