Gambaran Pengetahuan Dan Ketepatan Pemberian Makan Dengan Status Gizi Pada Baduta Umur 0-24 Bulan Di Desa Raknamo Kecamatan Amabi Oefeto Kabupaten Kupang

Latar Belakang : Terciptanya Indonesia yang sehat maka hal yang perlu diperbaiki adalah sumber daya manusia (SDM). Hal yang paling mendasar yang harus digerakkan dari awal yaitu pada anak-anak baduta , karena anak-anak Baduta merupakan generasi penerus bangsa yang menentukan maju mundurnya bangsa dimasa yang akan datang. Tujuan Penelitian: Untuk Mengetahui Gambaran Pengetahuan Ibu Dan Ketepatan Pemberian Makan Dengan Status Gizi Pada Baduta Umur 0-24 Bulan Di Desa Raknamo, Kecamatan Amabi Oefeto Kabupaten Kupang. Metode Penelitian:Jenis penelitian ini merupakan penelitian kualitatif dengan rancangan observasional deskriptif. Hasil penelitian: Berdasarkan hasil penelitian diketahui bahwa lebih banyak ibu yang memiliki pengetahuan kurang sebanyak 67 orang (81.7%) pengetahuan cukup sebanyak 14 orang (17.1%) dibandingkan ibu yang memiliki pengetahuan baik 1 orang (1.2%). Ketepatan waktu pemberian Asi-Eksklusif kategori baik sebanyak 12 orang (14.63%) dan kategori tidak baik sebanyak 70 orang (85.36%). Ketepatan waktu pemberian MP-Asi kategori baik sebanyak 7 orang (8.53%) dan kategori tidak baik sebanyak 75 orang (91.46). Kesimpulan: Pengetahuan ibu yang baik status gizi anak juga baik, pengetahuan ibu yang cukup, status gizi anak baik. Pengetahuan ibu yang kurang status gizi anak buruk. Hal ini menunjukan bahwa pengetahuan ibu yang baik akan mempengaruhi ketepatan pemberian makan dan status gizi anak

Intermediates in the assembly of mitotic checkpoint complexes and their role in the regulation of the anaphase-promoting complex

Significance The mitotic checkpoint system has important roles to ensure accurate segregation of chromosomes in mitosis. This system regulates the activity of the ubiquitin ligase Anaphase-Promoting Complex/Cyclosome (APC/C) by the formation of inhibitors including the Mitotic Checkpoint Complex (MCC). The mode of the assembly of MCC is not sufficiently understood, and it is also not known whether checkpoint complexes different from MCC also inhibit the APC/C. We find that complexes lacking Mad2, a protein component of MCC, have greatly reduced APC/C inhibitory action. On the other hand, a previously unknown species of MCC that contains an additional molecule of Cdc20 is a strong inhibitor of APC/C. These results reveal important molecular mechanisms in the action of the mitotic checkpoint system.</jats:p

Role of phosphorylation of Cdc20 in p31 ^comet -stimulated disassembly of the mitotic checkpoint complex

The mitotic checkpoint system delays anaphase until all chromosomes are correctly attached to the mitotic spindle. When the checkpoint is turned on, it promotes the formation of the mitotic checkpoint complex (MCC), which inhibits the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C). MCC is composed of the checkpoint proteins BubR1, Bub3, and Mad2 bound to the APC/C activator Cdc20. When the checkpoint is satisfied, MCC is disassembled and APC/C becomes active. Previous studies have shown that the Mad2-binding protein p31 comet promotes the dissociation of Cdc20 from BubR1 in MCC in a process that requires ATP. We now show that a part of MCC dissociation is blocked by inhibitors of cyclin-dependent kinases (Cdks) and that purified Cdk1–cyclin B stimulates this process. The mutation of all eight potential Cdk phosphorylation sites of Cdc20 partially prevented its release from BubR1. Furthermore, p31 comet stimulated Cdk-catalyzed phosphorylation of Cdc20 in MCC. It is suggested that the binding of p31 comet to Mad2 in MCC may trigger a conformational change in Cdc20 that facilitates its phosphorylation by Cdk, and that the latter process may promote its dissociation from BubR1. </jats:p

Role of ubiquitin-protein ligase UBR5 in the disassembly of mitotic checkpoint complexes

Significance The mitotic checkpoint system is essential for the prevention of mistakes in the segregation of chromosomes in mitosis. As long as chromosomes are not attached correctly to the mitotic spindle, a mitotic checkpoint complex (MCC) is assembled and inhibits the action of ubiquitin ligase APC/C (anaphase-promoting complex/cyclosome) to initiate anaphase. When the checkpoint is turned off, MCC is disassembled, allowing anaphase initiation. The mechanisms of MCC disassembly have been studied, but the regulation of this process remained obscure. We found that a second ubiquitin ligase, UBR5 (ubiquitin-protein ligase N -recognin 5), ubiquitylates MCC components and stimulates the disassembly of MCC from APC/C, as well as the dissociation of a subcomplex of MCC. </jats:p

p31 ^comet promotes disassembly of the mitotic checkpoint complex in an ATP-dependent process

Accurate segregation of chromosomes in mitosis is ensured by a surveillance mechanism called the mitotic (or spindle assembly) checkpoint. It prevents sister chromatid separation until all chromosomes are correctly attached to the mitotic spindle through their kinetochores. The checkpoint acts by inhibiting the anaphase-promoting complex/cyclosome (APC/C), a ubiquitin ligase that targets for degradation securin, an inhibitor of anaphase initiation. The activity of APC/C is inhibited by a mitotic checkpoint complex (MCC), composed of the APC/C activator Cdc20 bound to the checkpoint proteins MAD2, BubR1, and Bub3. When all kinetochores acquire bipolar attachment the checkpoint is inactivated, but the mechanisms of checkpoint inactivation are not understood. We have previously observed that hydrolyzable ATP is required for exit from checkpoint-arrested state. In this investigation we examined the possibility that ATP hydrolysis in exit from checkpoint is linked to the action of the Mad2-binding protein p31 comet in this process. It is known that p31 comet prevents the formation of a Mad2 dimer that it thought to be important for turning on the mitotic checkpoint. This explains how p31 comet blocks the activation of the checkpoint but not how it promotes its inactivation. Using extracts from checkpoint-arrested cells and MCC isolated from such extracts, we now show that p31 comet causes the disassembly of MCC and that this process requires β,γ-hydrolyzable ATP. Although p31 comet binds to Mad2, it promotes the dissociation of Cdc20 from BubR1 in MCC. </jats:p