Dwi Cahyani Ratna Sari
Departement Of Anatomy, Faculty Of Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia

Published : 23 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 23 Documents
Search

Angka Kejadian Hipertensi Pada Pemetik Teh Lansia di Kemuning, Karanganyar Setiorini, Anggi; Agustiningsih, Denny; Yunus, Junaedy
Muhammadiyah Journal of Geriatric Vol 2, No 2 (2021): Muhammadiyah Journal of Geriatric
Publisher : Faculty of Medicine and Health Universitas Muhammadiyah Jakarta

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24853/mujg.2.2.49-54

Abstract

Latar belakang: hipertensi mengakibatkan banyak masalah seperti penyakit kardiovaskular. Hipertensi dapat menurunkan kualitas kinerja seseorang dan mengganggu kualitas hidup. Hipertensi dapat terjadi pada semua usia tetapi paling banyak pada usia lansia karena lansia mengalami penurunan elastisitas pembuluh darah. Tujuan: tujuan penelitian ini untuk mengetahui angka kejadian dan hubungan hipertensi pada pemetik teh lansia yang berada di Perkebunan Teh Kemuning, Karanganyar meliputi umur, masa kerja, waktu kerja dan Indeks Masa Tubuh. Metode: cross sectional dengan sampel sejumlah 30 orang pemetik teh yang sudah berusia lansia, bekerja lebih dari 5 tahun, bekerja pada area kemiringan 450. Variabel yang diukur adalah hipertensi, masa kerja, waktu kerja, pendidikan, berat badan dan tinggi badan pemetik teh.Uji bivariat menggunakan Chi Square. Hasil: penelitian ini menunjukkan angka kejadian hipertensi ringan sebanyak 83,3% dan hipertensi sedang sebanyak 16,7%. Simpulan: penelitian ini adalah terdapat hubungan antara kejadian hipertensi baik ringan dan sedang terhadap umur dan masa kerja tetapi tidak terdapat hubungan antara waktu kerja dan IMT dengan kejadian hipertensi baik ringan maupun sedang karena pada sampel didapatkan bahwa IMT normal banyak. 
Cytoarchitectural changes in the developing cerebellar cortex of the laggard mutant mouse Yunus, Junaedy; Setsu, Tomiyoshi; Kikkawa, Satoshi; Terashima, Toshio
Narra J Vol. 5 No. 2 (2025): August 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narraj.v5i2.2075

Abstract

The laggard (lag) mutant mouse, which arises from a mutation in the Kif14 gene, begins to exhibit ataxia and impaired growth after the first postnatal week and subsequently dies prematurely around two weeks of age. In this mutant mouse, the layered architecture of the cerebellar cortex, cerebral cortex, dentate gyrus, and olfactory bulb is disrupted at the cellular level. The aim of this study was to identify the effect of Kif14 mutation on the development of the cerebellar cortex. Abnormalities in the cytoarchitectonics of the developing cerebellar cortex were assessed using hematoxylin-eosin (HE) staining and immunohistochemistry. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and bromodeoxyuridine (BrdU) assays were performed to identify apoptotic and proliferating cells. Macroscopic observation of the lag mutant cerebellum reveals a marked reduction in size compared to wild-type mice. HE staining displays a normal foliation and lamination pattern in the lag mutant cerebellum, but detailed analysis has shown morphological disorganization in the cytoarchitectonics of the cerebellar cortex. The mutant internal granular layer is poorly defined and contains significantly fewer granule cells. Meanwhile, Purkinje cells form multilayer arrangements instead of a monolayer arrangement, as observed in wild-type mice, with their dendritic arborization being severely underdeveloped. Some Purkinje cells exhibit multiple nuclei, suggesting that the Kif14 mutation disrupts normal cell division. These phenotypes are already recognized during early postnatal days, although no difference is determined before birth. TUNEL-positive cells are significantly more numerous in the mutant external granular layer, indicating that increased apoptotic cell death contributes to the diminished granule cell population in the lag mutant mouse. In conclusion, the lag mutant cerebellar cortex shows distinct structural abnormalities, suggesting that the Kif14-encoded protein exerts multifaceted roles in the development of the brain laminated structures as well as in myelin formation.
Role of nuclear factor-κB (NFκB) in microglial polarization in correlation with neuroinflammatory mechanism at the hippocampal cornu ammonis (CA) 1 region after acute and chronic phase of global ischemic brain injury in rats Wibisono, Dian Prasetyo; Nur Arfian; Fauziyatul Munawaroh; Dwi Cahyani Ratna Sari
Indonesian Journal of Biomedicine and Clinical Sciences Vol 57 No 3 (2025)
Publisher : Published by Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/inajbcs.v57i3.12757

Abstract

Ischemic brain injuries can result in hippocampal injury due to its vulnerability to ischemia, specifically the CA1 region. Ischemic injury to this region alters nerve cells, synapses, and non-neural hippocampal tissue and causes hippocampal sclerosis. This injury could be mediated by microglia via the neuroinflammation pathway. However, the neuroinflammatory mechanism underlying hippocampal ischemic injury is still unclear. This study aimed to investigate the role of NF-κB in microglia polarization which affects the hippocampal area after ischemic injury. We conducted a quasi-experimental study, using 24 male Sprague Dawley rats aged 4 wk old and weighing 100 g. The rats were grouped into 4 different groups (CL1 as acute, CL3 as subacute, CL7 as chronic, and SO as control groups) and performed bilateral common carotid artery ligation to induce global ischemic injury in the brain. The difference in microglial activation was tested using immunohistochemistry for CD68. Moreover, polymerase chain reaction (PCR) was utilized to assess mRNA expression differences in IL1β, IL6, TNFα, and NF-κB. An increase in the number of positive CD68 fraction areas in CL1, CL3, and CL7 compared to the SO group (p=0.002) was shown after bilateral common carotid artery ligation. Such ligation also induced a significantly higher mRNA expression of IL1β (p=0.004), IL6 (p=0.028), TNFα (p=0.028), and NF-κB (p=0.002) in the CL1, CL3, and CL7 groups, compared to the SO group. In conclusion, NF-κB is the key player in hippocampal injury in the CA1 region following ischemic event by differentiating microglia into M1 phenotype form and initiates the neuroinflammatory cascade via IL1β, IL6, and TNFα in all phases.