Asuhan Kebidanan Berkelanjutan Pada Ny U.R Puskesmas Sagu Periode 22 April sampai 29 Juni 2019

Latar Belakang : Penyusunan Laporan Tugas Akhir adalah kegiatan belajar mengajar yang memberikan kesempatan kepada mahasiswa untuk mendapatkan pengalaman nyata dalam melaksanakan asuhan kebidanan yang komprehensif dalam lingkup kesehatan reproduksi.Data Puskesmas Sagu diperoleh tidak ada kematian bayi dan kematian ibu dalam 1 tahun terakhir. Sasaran ibu hamil di Puskesmas Sagu sebanyak 178 orang, jumlah persalinan sebanyak 194 orang, jumlah kunjungan nifas sebanyak 193 orang. Tujuan Penelitian : Diharapkan mahasiswa mampu menerapkan asuhan kebidanan berkelanjutan pada Ny.U.R Usia Kehamilan 37 Minggu 2 Hari Janin Hidup Tunggal Letak Kepala Intra Uterine Keadaan Jalan Lahir Normal Keadaan Ibu dan Janin Baik di Puskesmas Sagu Periode 22 April sampai 29 Juni 2019. Metode Penelitian : Jenis penelitian yang digunakan adalah studi penelaahan kasus. Studi kasus dilakukan pada Ny.U.R Usia Kehamilan 37 Minggu 2 Hari Janin Tunggal Hidup Intra Uterine Letak Kepala Keadaan Ibu dan Janin Baik di PuskesmaS Sagu Periode 22 April sampai 29 Juni 2019. Hasil : Setelah dilakukan asuhan kebidanan berkelanjutan pada Ny. U.R Usia Kehamilan 37 minggu 2 Hari Janin Tunggal Hidup Intra Uterine Letak Kepala Keadaan Ibu dan Janin Baik di Puskesmas Sagu Periode 22 April sampai 29 Juni 2019, ibu sudah melewati masa kehamilan, persalinan dan nifas dengan baik tanpa ada penyulit, bayi baru lahir dalam keadaan sehat, ibu belum menggunakan KB karena masih menunggu persetujuan suami. Kesimpulan : Asuhan kebidanan yang dilakukan pada Ny U.R mulai dari hamil, bersalin, BBL dan nifas, serta KB tidak ditemukan adanya kelainan dan penyulit yang menyertai

TGFβR signalling determines CD103⁺CD11b⁺ dendritic cell development in the intestine

CD103+CD11b+ dendritic cells (DCs) are unique to the intestine, but the factors governing their differentiation are unclear. Here we show that transforming growth factor receptor 1 (TGFβR1) has an indispensable, cell intrinsic role in the development of these cells. Deletion of Tgfbr1 results in markedly fewer intestinal CD103+CD11b+ DCs and a reciprocal increase in the CD103−CD11b+ dendritic cell subset. Transcriptional profiling identifies markers that define the CD103+CD11b+ DC lineage, including CD101, TREM1 and Siglec-F, and shows that the absence of CD103+CD11b+ DCs in CD11c-Cre.Tgfbr1fl/fl mice reflects defective differentiation from CD103−CD11b+ intermediaries, rather than an isolated loss of CD103 expression. The defect in CD103+CD11b+ DCs is accompanied by reduced generation of antigen-specific, inducible FoxP3+ regulatory T cells in vitro and in vivo, and by reduced numbers of endogenous Th17 cells in the intestinal mucosa. Thus, TGFβR1-mediated signalling may explain the tissue-specific development of these unique DCs

Absence of MHC class II on cDCs results in microbial-dependent intestinal inflammation.

Conventional dendritic cells (cDCs) play an essential role in host immunity by initiating adaptive T cell responses and by serving as innate immune sensors. Although both innate and adaptive functions of cDCs are well documented, their relative importance in maintaining immune homeostasis is poorly understood. To examine the significance of cDC-initiated adaptive immunity in maintaining homeostasis, independent of their innate activities, we generated a cDC-specific Cre mouse and crossed it to a floxed MHC class II (MHCII) mouse. Absence of MHCII on cDCs resulted in chronic intestinal inflammation that was alleviated by antibiotic treatment and entirely averted under germ-free conditions. Uncoupling innate and adaptive functions of cDCs revealed that innate immune functions of cDCs are insufficient to maintain homeostasis and antigen presentation by cDCs is essential for a mutualistic relationship between the host and intestinal bacteria

Rapid fucosylation of intestinal epithelium sustains host–commensal symbiosis in sickness

Systemic infection induces conserved physiological responses that include both resistance and ‘tolerance of infection’ mechanisms. Temporary anorexia associated with an infection is often beneficial, reallocating energy from food foraging towards resistance to infection or depriving pathogens of nutrients. However, it imposes a stress on intestinal commensals, as they also experience reduced substrate availability; this affects host fitness owing to the loss of caloric intake and colonization resistance (protection from additional infections). We hypothesized that the host might utilize internal resources to support the gut microbiota during the acute phase of the disease. Here we show that systemic exposure to Toll-like receptor (TLR) ligands causes rapid α(1,2)-fucosylation of small intestine epithelial cells (IECs) in mice, which requires the sensing of TLR agonists, as well as the production of interleukin (IL)-23 by dendritic cells, activation of innate lymphoid cells and expression of fucosyltransferase 2 (Fut2) by IL-22-stimulated IECs. Fucosylated proteins are shed into the lumen and fucose is liberated and metabolized by the gut microbiota, as shown by reporter bacteria and community-wide analysis of microbial gene expression. Fucose affects the expression of microbial metabolic pathways and reduces the expression of bacterial virulence genes. It also improves host tolerance of the mild pathogen Citrobacter rodentium. Thus, rapid IEC fucosylation appears to be a protective mechanism that utilizes the host’s resources to maintain host–microbial interactions during pathogen-induced stress

Structures of vertebrate Patched and Smoothened reveal intimate links between cholesterol and Hedgehog signalling

The Hedgehog (HH) signalling pathway is a cell–cell communication system that controls the patterning of multiple tissues during embryogenesis in metazoans. In adults, HH signals regulate tissue stem cells and regenerative responses. Abnormal signalling can cause birth defects and cancer. The HH signal is received on target cells by Patched (PTCH1), the receptor for HH ligands, and then transmitted across the plasma membrane by Smoothened (SMO). Recent structural and biochemical studies have pointed to a sterol lipid, likely cholesterol itself, as the elusive second messenger that communicates the HH signal between PTCH1 and SMO, thus linking ligand reception to transmembrane signalling