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Kadar Glukosa Darah Sapi Bali Tidak Bunting di Sentra Pembibitan Sapi Bali Sobangan, Badung, Bali Purwitasari, Made Santi; Widyastuti, Sri Kayati; Erawan, I Gusti Made Krisna
Indonesia Medicus Veterinus Vol 9 (6) 2020
Publisher : Faculty of Veterinary Medicine, Udayana University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19087/imv.2020.9.6.870

Abstract

Glukosa merupakan monosakarida yang dibutuhkan dalam jumlah yang banyak oleh sapi bali untuk kebutuhan hidup pokok, pertumbuhan tubuh, pertumbuhan fetus, pertumbuhan jaringan tubuh dan produksi susu. Rendahnya glukosa darah dapat menyebabkan penurunan produktivitas sapi bali terutama sapi bali betina. Penelitian ini bertujuan untuk mengetahui status kesehatan ternak sapi bali dengan cara menghitung kadar glukosa darah sapi bali betina tidak bunting di Sentra Pembibitan Sapi Bali Desa Sobangan, Kecamatan Mengwi, Kabupaten Badung. Penelitian ini menggunakan sampel darah 12 ekor sapi bali betina tidak bunting dengan umur di atas dua tahun dan secara klinis sehat. Sampel darah diambil melalui vena jugularis menggunakan venoject berukuran 21G. Darah diambil dua kali yaitu sebelum pemberian pakan (0 jam) dan 2 jam setelah pemberian pakan. Sampel darah diperiksa menggunakan glukometer Nesco Multicheck 3 in 1 (glukosa, asam urat, dan kolestrol). Hasil penelitian menunjukkan rerata kadar glukosa darah yang sangat berbeda antara sapi bali tidak bunting pada waktu sebelum pemberian pakan (0 jam) yaitu 43,11 ± 2.98 mg/dL dan pada 2 jam setelah pemberian pakan yaitu 66,44 ± 2.87 mg/dL.
LAPORAN KASUS: KESEMBUHAN ENTERITIS HEMORAGIKA PADA ANAK ANJING KACANG YANG TERINFEKSI CANINE PARVOVIRUS Purwitasari, Made Santi; Soma, I Gede; Batan, I Wayan
JURNAL KAJIAN VETERINER Vol 10 No 1 (2022): Jurnal Kajian Veteriner
Publisher : FAKULTAS KEDOKTERAN HEWAN UNIVERSITAS NUSA CENDANA

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.35508/jkv.v10i1.6290

Abstract

Canine parvovirus (CPV) is an infectious disease with clinical signs of bloody diarrhea (hemorrhagic enteritis) which is cause of death in infected dogs. A five-month-old female local dog with a weight of 4.3 kg, black and white coat on the ventral side came to the Rumah Sakit Hewan Pendidikan, Faculty of Veterinary Medicine, Udayana University with complaints of weakness, loss of appetite since the day before and vomiting in the morning of the examination. The dog is rescued and never been vaccinated before. Clinical examination showed weakness such as holding pain, pink pale eye mucosae, delayed skin turgor, Capillary Refill Time (CRT) more than two seconds, and increased respiratory rate. Dogs do not respond to handfeeding. On observation the dog experienced clear and foamy vomiting and foul-smelling bloody diarrhea. The native stool faecal examination showed negative results, while the CPV antigen rapid test examination showed positive results. Complete blood count showed that on the first day of hospitalization the dog had leukopenia, granulocytopenia, hyperchromic normocytic anemia and thrombocytopenia. The dog was diagnosed with CPV with a dubious prognosis. Dogs were given fluid therapy using sodium chloride 0.9% infusion and vitamin B complex, anti-emetic ondansetron, antibiotic cefotaxime, and vitamin K. Dogs were also treated with traditional medicine Fu Fang 1 mL and trigona honey 1 mL. Dogs are given a special feed Hills Prescription Diet A/D Urgent Care. The dog's condition improved after offering therapy for seven days and the dog was declared cured and could be sent home on the ninth day.
The Role of p53 as the Guardian of the Genome and the Consequences of its Mutation in Cancer Development: A Review Purwitasari, Made Santi; Sewoyo, Palagan Senopati; Astawa, I Nyoman Mantik
Jurnal Medika Veterinaria Vol 19, No 2 (2025): J.Med.Vet
Publisher : Universitas Syiah Kuala

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21157/j.med.vet..v19i2.48988

Abstract

The TP53 gene encodes the p53 protein, often referred to as the guardian of the genome due to its critical role in maintaining genomic stability and preventing tumorigenesis. Under normal conditions, p53 expression is tightly regulated by MDM2 and MDMX, which promote its degradation through ubiquitination. In response to endogenous or exogenous stress, this ubiquitination process is inhibited, leading to the stabilization of p53. Once stabilized, p53 forms a tetrameric complex in the nucleus and binds to DNA. It then activates the transcription of genes involved in cell cycle arrest, DNA repair, apoptosis, and senescence, aiming either to repair DNA damage or eliminate cells when the damage is irreparable. Nearly half of all cancer cases involve mutations in the TP53 gene. These mutations may include missense, nonsense, inframe, and splice-site mutations. Mutations in TP53 result in the production of mutant p53 (mutp53) proteins. These mutations can lead to a loss of tumor suppressor function or confer gain-of-function properties that promote tumor progression. Given its central role in cancer development, TP53 is considered a promising therapeutic target. Potential strategies include reactivating suppressed p53, restoring the function of mutp53, or inducing its degradation.