Biology subjects

Kurniawan, N. D.

Publications and source records attributed to Kurniawan, N. D..

4 recordsLinked to original sources

bioRxiv2026

Synchrotron phase contrast micro-CT of prostate tissue

Formalin-fixed prostate tissue samples were imaged by propagation-based synchrotron phase contrast micro computed tomography ({micro}CT) with a 3D spatial resolution of ca. 3 {micro}m. Post-{micro}CT, samples were prepared for histology with sections close to coplanar with the transverse {micro}CT image planes. Haematoxylin and eosin stained sections were examined by an expert prostate histopathologist and compared qualitatively with corresponding {micro}CT-visible microstructure features. There is potential for {micro}CT to provide complimentary information to conventional histology and light microscopy without the need for preparation of stained thin sections. For the imaging conditions and spatial resolution of our study, {micro}CT may provide tissue architectural features similar to those used in Gleason grading, albeit without clear subcellular microstructure detail. At the spatial resolution of our study {micro}CT may provide novel 3D microstructure information for validation of diffusion weighted magnetic resonance imaging (MRI) methods. As an example, we demonstrate a qualitative correlation between {micro}CT-derived stromal fibre orientation and preferential water diffusion direction measured by diffusion tensor MRI microscopy of the same sample.

cancer biology↗

bioRxiv2025

Mutation in the rat interleukin 34 gene impacts macrophage development, homeostasis and inflammation in the brain and periphery

Interleukin-34 (IL34) and colony stimulating factor 1 (CSF1) signal through a shared receptor (CSF1R) to control macrophage survival, differentiation and function. Here we describe the impact of loss of function mutation in the rat Il34 gene. Il34-/- rats showed a partial reduction in macrophages within squamous epithelia (Langerhans-like cells) and in the testis. In the brain, microglia and brain-associated macrophages were selectively depleted in grey matter. A gradient of microglial density in Il34-/- cortex suggests that CSF1 can diffuse outwards from the corpus callosum. The reduced density of microglia was not associated with detectable neuropathology or behavioural alterations. In RNA-seq analysis of cortex, hippocampus and thalamus the only change is selective and uniform loss of the microglial signature. In the periphery, increased Il34 expression has been associated with epithelial injury. In the adenine diet model of renal interstitial fibrosis both Il34 and Csf1 were induced. The absence of IL34 led to a significant reduction in macrophage recruitment compared to controls, but pathology assessed histologically or by detection of damage-associated mRNA signature was unaffected. We suggest that IL34 and CSF1 provide redundant signals to sustain microglia and to direct macrophage recruitment and repair tissue injury in the periphery.

immunology↗

bioRxiv2025

Repopulation of the brain with microglia-like cells following intraperitoneal bone marrow cell transfer in microglia-deficient mice.

Germ-line deletion of a conserved enhancer (the Fms intrinsic regulatory element, FIRE) in the mouse Csf1r locus causes congenital absence of microglia. Homozygous FIRE deletion on a C57BL/6J background leads to perinatal lethality and hydrocephalus (HC) in surviving pups. We developed a congenic C57BL/6J line with defined regions of non-C57BL/6J genomic DNA, increased postnatal viability and reduced incidence of HC. Both perinatal lethality and HC were eliminated in F2 mice following outcross of the congenic line to CBA/J or BALBc/J backgrounds. To assess the impacts of microglial deficiency in postnatal neurodevelopment we analyzed deep total RNA-seq data from multiple brain regions of wild-type and Csf1r{Delta}FIRE/{Delta}FIRE mice. Aside from the loss of microglial-specific transcripts, we found no significant alterations in relative abundance of any cell-type or region-specific transcriptomic signature. Transcripts associated with endosome/lysosome function, which are enriched in microglia, were not affected, suggesting compensatory expression by other cell types. On the C57BL/6J x CBA/J F2 background, congenital absence of microglia did not affect motor activity, behavior or myelination up to 7 months of age but was associated with astrocytosis and calcification in the thalamus. In the congenic C57BL/6J Csf1r{Delta}FIRE/{Delta}FIRE mouse line, intraperitoneal transfer of wild-type bone marrow cells (BMT) at weaning led to complete repopulation of the brain with microglia-like cells without giving rise to monocytic intermediates. Our results suggest novel strategies for treatment of microglial deficiency.

neuroscience↗

bioRxiv2019

Homologous laminar organization of the mouse and human subiculum

The subiculum is the major output structure of the hippocampal formation and one of the brain regions most affected by Alzheimers disease. Our previous work revealed a hidden laminar architecture within the mouse subiculum. However, the rotation of the hippocampal longitudinal axis across species makes it unclear how the laminar organization is represented in human subiculum. Using in situ hybridization data from the Allen Human Brain Atlas, we demonstrate that the human subiculum also contains complementary laminar gene expression patterns similar to the mouse. In addition, we provide evidence that the molecular domain boundaries in human subiculum correspond to microstructural differences observed in high resolution MRI and fiber density imaging. Finally, we show both similarities and differences in the gene expression profile of subiculum pyramidal cells within homologous lamina. Overall, we present a new 3D model of the anatomical organization of human subiculum and its evolution from the mouse.

neuroscience↗