HUBUNGAN ANTARA TINGKAT PENGETAHUAN IBU TENTANG PENTINGNYA ANTENATAL CARE DENGAN KETERATURAN ANTENATAL CARE DI BPS MIMIEK ANDAYANI SIMO POMAHAN SURABAYA

Pemeriksaan kehamilan secara teratur sangat penting guna memantau kesehatan ibu dan janin. Survey awal pada januari-mei 2012 di BPS Ny. Mimiek Andayani sebesar 61%, target tersebut masih jauh dari target yang telah ditetapakan Depkes. RI yaitu 95 %. Faktor yang mempengaruhi keteraturan salah satunya pengetahuan, Penelitian ini bertujuan untuk mengetahui Hubungan Tingkat Pengetahuan Ibu tentang Pentingnya ANC dengan Keteraturan ANC. Desain penelitian ini adalah analitik dengan metode cross sectional. Populasi semua ibu hamil trimester III yang memeriksakan kehamilan di BPS Mimiek Andayani sebanyak 34 responden, pengambilan sampel dengan teknik “Simple Random Sampling” besar sampel sebanyak 31 responden. Instrumen yang digunakan menggunakan kuesioner, Variabel independent adalah tingkat pengetahuan, variabel dependent adalah keteraturan antenatal care dan dianalisa menggunakan uji Mann Whitney dengan program SPSS for windows. Hasil penelitian menunjukan bahwa hampir setengahnya responden memiliki pengetahuan kurang (35,48%) dan sebagian besar (51,6%) teratur melakukan antenatal care, Hasil statistik dengan angka kemaknaan α = 0,05 diperoleh hasil ρ = 0,001 sehingga ρ < α, maka Ho ditolak berarti ada hubungan Tingkat Pengetahuan Ibu tentang Pentingnya ANC dengan Keteraturan ANC. . Simpulan penelitian ini adalah sebagian besar responden mempunyai pengetahuan kurang tentang pentingnya ANC sehingga berpengaruh pada keteraturan pemeriksaan ANC. Oleh karena itu disarankan petugas kesehatan aktif dalam memberikan penyuluhan tentang pentingnya antenatal care

MEMBANGUN INTEGRITAS PADA ANAK-ANAK USIA DINI DI DESA BUNUT SEBRANG

Kreativitas adalah kemampuan untuk memikirkan sesuatu dengan cara yang baru dan tidak biasa serta melahirkan solusi yang unik terhadap masalah yang dihadapi. Peran kreativitas semakin terasa ketika memasuki abad 21 dengan ditandai oleh perubahan yang sangat cepat dan tantangan yang semakin kompleks. Sehingga kreativitas harus dikembangkan sejak dini melalui pembelajaran yang dilakukan secara terintegrasi.Penelitian ini membahas tentang bagaimana cara membangun integeritas anak usia dini di desa Bunut Seberang. Penelitian ini merupakan penelitian deskriptif kualitatif dengan observasi, wawancara dan eksperimen. Aktivitas meliputi pembelajaran dan penyuluhan di SDN 015861 Bunut Seberang. Kata Kunci : Deskriptif  Kualitatif, Integeritas, Kreativitas

NLRP3 and ASC suppress lupus-like autoimmunity by driving the immunosuppressive effects of TGF-beta receptor signalling

Objectives: The NLRP3/ASC inflammasome drives host defence and autoinflammatory disorders by activating caspase-1 to trigger the secretion of mature interleukin (IL)-1β/IL-18, but its potential role in autoimmunity is speculative. Methods: We generated and phenotyped Nlrp3-deficient, Asc-deficient, Il-1r-deficient and Il-18-deficient C57BL/6-lpr/lpr mice, the latter being a mild model of spontaneous lupus-like autoimmunity. Results: While lack of IL-1R or IL-18 did not affect the C57BL/6-lpr/lpr phenotype, lack of NLRP3 or ASC triggered massive lymphoproliferation, lung T cell infiltrates and severe proliferative lupus nephritis within 6 months, which were all absent in age-matched C57BL/6-lpr/lpr controls. Lack of NLRP3 or ASC increased dendritic cell and macrophage activation, the expression of numerous proinflammatory mediators, lymphocyte necrosis and the expansion of most T cell and B cell subsets. In contrast, plasma cells and autoantibody production were hardly affected. This unexpected immunosuppressive effect of NLRP3 and ASC may relate to their known role in SMAD2/3 phosphorylation during tumour growth factor (TGF)-β receptor signalling, for example, Nlrp3-deficiency and Asc-deficiency significantly suppressed the expression of numerous TGF-β target genes in C57BL/6-lpr/lpr mice and partially recapitulated the known autoimmune phenotype of Tgf-β1-deficient mice. Conclusions: These data identify a novel non-canonical immunoregulatory function of NLRP3 and ASC in autoimmunity

Quantitative Expression of C-Type Lectin Receptors in Humans and Mice

C-type lectin receptors, their adaptor molecules and S-type lectins (galectins) are involved in the recognition of glycosylated self-antigens and pathogens. However, little is known about the species- and organ-specific expression profiles of these molecules. We therefore determined the mRNA expression levels of Dectin-1, MR1, MR2, DC-SIGN, Syk, Card-9, Bcl-10, Malt-1, Src, Dec-205, Galectin-1, Tim-3, Trem-1, and DAP-12 in 11 solid organs of human and mice. Mouse organs revealed lower mRNA levels of most molecules compared to spleen. However, Dec-205 and Galectin-1 in thymus, Src in brain, MR2, Card-9, Bcl-10, Src, and Dec-205 in small intestine, MR2, Bcl-10, Src, Galectin-1 in kidney, and Src and Galectin-1 in muscle were at least 2-fold higher expressed compared to spleen. Human lung, liver and heart expressed higher mRNA levels of most genes compared to spleen. Dectin-1, MR1, Syk and Trem-1 mRNA were strongly up-regulated upon ischemia-reperfusion injury in murine kidney. Tim3, DAP-12, Card-9, DC-SIGN and MR2 were further up-regulated during renal fibrosis. Murine kidney showed higher DAP-12, Syk, Card-9 and Dectin-1 mRNA expression during the progression of lupus nephritis. Thus, the organ-, and species-specific expression of C-type lectin receptors and galectins is different between mice and humans which must be considered in the interpretation of related studies

Toll-Like Receptor Signaling and SIGIRR in Renal Fibrosis upon Unilateral Ureteral Obstruction

Innate immune activation via IL-1R or Toll-like receptors (TLR) contibutes to acute kidney injury but its role in tissue remodeling during chronic kidney disease is unclear. SIGIRR is an inhibitor of TLR-induced cytokine and chemokine expression in intrarenal immune cells, therefore, we hypothesized that Sigirr-deficiency would aggravate postobstructive renal fibrosis. The expression of TLRs as well as endogenous TLR agonists increased within six days after UUO in obstructed compared to unobstructed kidneys while SIGIRR itself was downregulated by day 10. However, lack of SIGIRR did not affect the intrarenal mRNA expression of proinflammatory and profibrotic mediators as well as the numbers of intrarenal macrophages and T cells or morphometric markers of tubular atrophy and interstitial fibrosis. Because SIGIRR is known to block TLR/IL-1R signaling at the level of the intracellular adaptor molecule MyD88 UUO experiments were also performed in mice deficient for either MyD88, TLR2 or TLR9. After UUO there was no significant change of tubular interstitial damage and interstitial fibrosis in neither of these mice compared to wildtype counterparts. Additional in-vitro studies with CD90+ renal fibroblasts revealed that TLR agonists induce the expression of IL-6 and MCP-1/CCL2 but not of TGF-β, collagen-1α or smooth muscle actin. Together, postobstructive renal interstitial fibrosis and tubular atrophy develop independent of SIGIRR, TLR2, TLR9, and MyD88. These data argue against a significant role of these molecules in renal fibrosis

Lack of the Long Pentraxin PTX3 Promotes Autoimmune Lung Disease but not Glomerulonephritis in Murine Systemic Lupus Erythematosus

The long pentraxin PTX3 has multiple roles in innate immunity. For example, PTX3 regulates C1q binding to pathogens and dead cells and regulates their uptake by phagocytes. It also inhibits P-selectin-mediated recruitment of leukocytes. Both of these mechanisms are known to be involved in autoimmunity and autoimmune tissue injury, e.g. in systemic lupus erythematosus, but a contribution of PTX3 is hypothetical. To evaluate a potential immunoregulatory role of PTX3 in autoimmunity we crossed Ptx3-deficient mice with Fas-deficient (lpr) C57BL/6 (B6) mice with mild lupus-like autoimmunity. PTX3 was found to be increasingly expressed in kidneys and lungs of B6lpr along disease progression. Lack of PTX3 impaired the phagocytic uptake of apoptotic T cells into peritoneal macrophages and selectively expanded CD4/CD8 double negative T cells while other immune cell subsets and lupus autoantibody production remained unaffected. Lack of PTX3 also aggravated autoimmune lung disease, i.e. peribronchial and perivascular CD3+ T cell and macrophage infiltrates of B6lpr mice. In contrast, histomorphological and functional parameters of lupus nephritis remained unaffected by the Ptx3 genotype. Together, PTX3 specifically suppresses autoimmune lung disease that is associated with systemic lupus erythematosus. Vice versa, loss-of-function mutations in the Ptx3 gene might represent a genetic risk factor for pulmonary (but not renal) manifestations of systemic lupus or other autoimmune diseases