Peran Guru Pendidikan Kewarganegaraan dalam Meningkatkan Rasa Nasionalisme pada Siswa Sekolah Dasar

Nasionalisme adalah nilai luhur Pancasila yang perlu dimiliki peserta didik sebagai generasi penerus bangsa untuk mengisi kemerdekaan dan mampu memberikan kontribusi bagi negara sehingga dapat terwujud karakter peserta didik yang dapat berdaya saing dan tangguh di tengah era globalisasi. Tujuan dari penelitian ini adalah untuk mengetahui peran guru pendidikan kewarganegaraan dalam meningkatkan rasa nasionalisme pada siswa sekolah dasar. Metode yang digunakan dalam penelitian ini yaitu metode penelitian dengan pendekatan kualitatif yang bersifat deskrifptif. Teknik pengumpulan data dilakukan dengan cara studi literatur dari berbagai sumber seperti buku, jurnal dan yang lainnya. Hasil penelitian yang diperoleh menunjukkan bahwa peran guru pendidikan kewarganegaraan sangat penting dalam meningkatkan sikap nasionalisme  pada siswa sekolah dasar yaitu Guru pendidikan kewarganegaraan sebagai pembimbing, Guru PPKn sebagai jembatan antar generasi, Guru pendidikan kewarganegaraan sebagai Stimulus kreativitas dan Guru pendidikan kewarganegaraan sebagai Otoritas. Sedangkan bentuk sikap Nasionalisme pada siswa sekolah dasar sebagai berikut: Sikap Nasionalisme dalam hal bangga menjadi bangsa Indonesia, Sikap Nasionalisme dalam hal rela berkorban, Sikap Nasionalisme dalam hal menerima kemajemukan dan Sikap Nasionalisme dalam hal menghargai jasa para pahlawan. &nbsp

PROBIOTIC LACTOBACILLUS REUTERI EFFECT’S ON THE LEVELS OF INTERLEUKIN-4 IN PERIODONTITIS PATIENTS AFTER SCALING AND ROOT PLANING

Objective: Periodontal disease is an inflammatory disease principally caused by a complex interaction between pathogenic bacteria and immuneresponses. Probiotics stimulate the immune system of the oral mucosa by increasing the production of anti-inflammatory cytokines. Interleukin-4 (IL-4) isthe anti-inflammatory cytokine that is most closely associated with the pathogenesis of periodontitis. This study assessed the effect of Lactobacillus reuteri(L. reuteri) containing probiotic lozenges toward clinical attachment loss (CAL) and IL-4 levels in periodontitis patients after scaling and root planing.Materials and Methods: Clinical samples were collected from the gingival crevicular fluid of 16 periodontitis patients with pocket depth (PD) of6 mm. The samples were divided into two groups. The non-probiotic group included periodontitis patients treated through scaling and root planing(SRP) only (n=8), whereas the probiotic group included periodontitis patients treated through SRP and probiotics (n=8). The measurements of theclinical parameters of PD and CAL were included as diagnostic criteria. Probiotic lozenges were given daily for 14 days. IL-4 levels were measured inboth groups using the enzyme-linked immunosorbent assay (ELISA) method.Results: IL-4 levels decreased in the non-probiotic group and increased in the probiotic group, but there was no statistical difference between thegroups. CAL decreased in both groups and was significantly different.Conclusion: SRP with the consumption of probiotic-containing L.reuteri in periodontitis patients resulted in decreased CAL and increased IL-4 levelscompared with SRP only

Impaired chemotaxis and cell adhesion due to decrease in several cell-surface receptors in cathepsin E-deficient macrophages.

Cathepsin E is an endo-lysosomal aspartic proteinase exclusively present in immune system cells. Previous studies have shown that cathepsin E-deficient (CatE(-/-)) mice display aberrant immune responses such as atopic dermatitis and higher susceptibility to bacterial infection. However, the mechanisms underlying abnormal immune responses induced by cathepsin E deficiency are still unclear. In this study, we found that the cell-surface levels of chemotactic receptors, including chemokine receptor (CCR)-2 and N-formyl peptide receptors (FPRs), were clearly diminished in CatE(-/-)macrophages compared with those in wild-type cells. Consistently, chemotaxis of CatE(-/-)macrophages to MCP-1 and N-formyl-methionyl-leucyl-phenylalanine was also decreased. Similar to the chemotactic receptors, the surface expressions of the adhesion receptors CD18 (integrin beta(2)) and CD 29 (integrin beta(1)) in CatE(-/-) macrophages were significantly decreased, thereby reducing cell attachment of CatE(-/-) macrophages. These results indicate that the defects in chemotaxis and cell adhesion are likely to be involved in the imperfect function of CatE(-/-)macrophages

Cathepsin E Deficiency Impairs Autophagic Proteolysis in Macrophages

Cathepsin E is an endosomal aspartic proteinase that is predominantly expressed in immune-related cells. Recently, we showed that macrophages derived from cathepsin E-deficient (CatE-/-) mice display accumulation of lysosomal membrane proteins and abnormal membrane trafficking. In this study, we demonstrated that CatE-/- macrophages exhibit abnormalities in autophagy, a bulk degradation system for aggregated proteins and damaged organelles. CatE-/- macrophages showed increased accumulation of autophagy marker proteins such as LC3 and p62, and polyubiquitinated proteins. Cathepsin E deficiency also altered autophagy-related signaling pathways such as those mediated by the mammalian target of rapamycin (mTOR), Akt, and extracellular signal-related kinase (ERK). Furthermore, immunofluorescence microscopy analyses showed that LC3-positive vesicles were merged with acidic compartments in wild-type macrophages, but not in CatE-/- macrophages, indicating inhibition of fusion of autophagosome with lysosomes in CatE-/- cells. Delayed degradation of LC3 protein was also observed under starvation-induced conditions. Since the autophagy system is involved in the degradation of damaged mitochondria, we examined the accumulation of damaged mitochondria in CatE-/- macrophages. Several mitochondrial abnormalities such as decreased intracellular ATP levels, depolarized mitochondrial membrane potential, and decreased mitochondrial oxygen consumption were observed. Such mitochondrial dysfunction likely led to the accompanying oxidative stress. In fact, CatE-/- macrophages showed increased reactive oxygen species (ROS) production and up-regulation of oxidized peroxiredoxin-6, but decreased antioxidant glutathione. These results indicate that cathepsin E deficiency causes autophagy impairment concomitantly with increased aberrant mitochondria as well as increased oxidative stress

Comparative study of microglia activation induced by amyloid-beta and prion peptides: Role in neurodegeneration

The inflammatory responses in Alzheimer's disease (AD) and prion-related encephalopathies (PRE) are dominated by microglia activation. Several studies have reported that the amyloid-beta (Abeta) peptides, which are associated with AD, and the pathogenic isoform of prion protein (PrPSc) have a crucial role in neuronal death and gliosis that occur in both of these disorders. In this study, we investigate whether Abeta and PrPSc cause microglia activation per se and whether these amyloidogenic peptides differentially affect these immunoeffector cells. In addition, we also determined whether substances released by Abeta- and PrP-activated microglia induce neuronal death. Cultures of rat brain microglia cells were treated with the synthetic peptides Abeta1-40, Abeta1-42 and PrP106-126 for different time periods. The lipopolysaccharide was used as a positive control of microglia activation. Our results show that Abeta1-40 and PrP106-126 caused similar morphological changes in microglia and increased the production of nitric oxide and hydroperoxides. An increase on inducible nitric oxide synthase expression was also observed in microglia treated with Abeta1-40 or PrP106. However, these peptides affected in a different manner the secretion of interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) secretion. In cocultures of microglia-neurons, it was observed that microglia treated with Abeta1-40 or PrP106-126 induced a comparable extent of neuronal death. The neutralizing antibody for IL-6 significantly reduced the neuronal death induced by Abeta- or PrP-activated microglia. Taken together, the data indicate that Abeta and PrP peptides caused microglia activation and differentially affected cytokine secretion. The IL-6 released by reactive microglia caused neuronal injury. © 2006 Wiley-Liss, Inc

Involvement of lysosomal storage-induced p38 MAP kinase activation in the overproduction of nitric oxide by microglia in cathepsin D-deficient mice

Yamasaki R, Zhang J, Koshiishi I, et al. Involvement of lysosomal storage-induced p38 MAP kinase activation in the overproduction of nitric oxide by microglia in cathepsin D-deficient mice. Molecular and Cellular Neuroscience. 2007;35(4):573-584.Nitric oxide (NO) and peroxynitrite, which are produced by activated microglia, are responsible for accelerated neurodegeneration in cathepsin D-deficient (CD−/−) mice. To elucidate the mechanisms by which microglia are initially activated in CD−/− mice, we analyzed the possible relationship between lysosomal storage and microglial activation. In CD−/− mice, the microglial NO-generating activity that was closely associated with the induction of inducible NO synthase and the cationic amino acid transporter-2 (CAT-2) coincided well with the lysosomal storage of subunit c of mitochondrial F0F1ATPase and the formation of ceroid/lipofuscin. Furthermore, activated microglia, which are often accumulating subunit c and ceroid/lipofuscin, showed proliferation activity and an activation of p38 mitogen-activated protein (MAP) kinase. In the primary cultured microglia, pepstatin A was found to enhance the generation of NO and superoxide anion radicals. In these pepstatin A-treated microglia, both an increased generation of the intracellular reactive oxygen species (ROS) and an activation of p38 MAP kinase were observed. These results suggest that the ceroid/lipofuscin which form in microglia activate the p38 MAP kinase cascade through the increased intracellular generation of ROS in CD−/− mice. The activated p38 MAP kinase cascade then promotes the expression of iNOS and CAT-2, thereby inducing the overproduction of NO