Publications by authors named "Ho Ching Chang"

Article Synopsis
  • * Research on Dlgap2 mutant mice showed that while their overall odor detection was similar to normal mice, they showed less interest in certain smells (banana and almond) but reacted more to unfamiliar bedding smells.
  • * The absence of DLGAP2 protein in Homo mutant mice affected their brain's response to odors, which suggests altered synaptic signaling in their olfactory systems and could inform future strategies for diagnosing and treating ASD-related olfactory issues.
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Cellular communication network factor 2 (CCN2) is a matricellular protein that plays important roles in connective tissue. CCN2 is also expressed in the nervous system; however, its role is still unclear. To explore CCN2 function in the brain, we generated forebrain-specific knockout (Fb KO) mice.

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A microdeletion of approximately 2.4 Mb at the 8p23 terminal region has been identified in a Taiwanese autistic boy. Among the products transcribed/translated from genes mapped in this region, the reduction of DLGAP2, a postsynaptic scaffold protein, might be involved in the pathogenesis of autism spectrum disorder (ASD).

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Mood disorders are an important public health issue and recent advances in genomic studies have indicated that molecules involved in neurodevelopment are causally related to mood disorders. BLM-s (BCL-2-like molecule, small transcript isoform), a BH3-only proapoptotic BCL-2 family member, mediates apoptosis of postmitotic immature neurons during embryonic cortical development, but its role in the adult brain is unknown. To better understand the physiological role of Blm-s gene in vivo, we generated a Blm-s-knockout (Blm-s) mouse.

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Connective tissue growth factor (CTGF) plays important roles in the development and regeneration of the connective tissue, yet its function in the nervous system is still not clear. CTGF is expressed in some distinct regions of the brain, including the dorsal endopiriform nucleus (DEPN) which has been recognized as an epileptogenic zone. We generated a forebrain-specific knockout (Fb KO) mouse line in which the expression of Ctgf in the DEPN is eliminated.

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PHRF1 is involved in transforming growth factor β (TGF-β) signaling to constrain the formation of acute promyelocytic leukemia (APL) in mouse APL models. PHRF1 also participates in modulating non-homologous end-joining. However, the role of PHRF1 in mammalian dendrite architecture and synaptic plasticity is unclear.

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Myotonic dystrophy (Dystrophia Myotonica; DM) is the most common adult-onset muscular dystrophy and its brain symptoms seriously affect patients' quality of life. It is caused by extended (CTG) expansions at 3'-UTR of gene (DM type 1, DM1) or (CCTG) repeats in the intron 1 of gene (DM type 2, DM2) and the sequestration of Muscleblind-like (MBNL) family proteins by transcribed (CUG) RNA hairpin is the main pathogenic mechanism for DM. The MBNL proteins are splicing factors regulating posttranscriptional RNA during development.

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Connective tissue growth factor (CTGF) is a secreted extracellular matrix-associated protein, which play a role in regulating various cellular functions. Although the expression of CTGF has been reported in the cortical subplate, its function is still not clear. Thus, to explore the significance of CTGF in the brain, we created a forebrain-specific knockout (Fb KO) mouse model.

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Vilse/Arhgap39 is a Rho GTPase activating protein (RhoGAP) and utilizes its WW domain to regulate Rac/Cdc42-dependent morphogenesis in Drosophila and murine hippocampal neurons. However, the function of Vilse in mammalian dendrite architecture and synaptic plasticity remained unclear. In the present study, we aimed to explore the possible role of Vilse in dendritic structure and synaptic function in the brain.

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Background: PPARγ and RBP4 are known to regulate lipid and glucose metabolism and insulin resistance. The influences of PPARγ (C1431T and Pro12Ala) and RBP4 (-803GA) polymorphisms on metabolic syndrome in HIV-infected patients receiving anti-retroviral therapy were examined in this study.

Materials And Methods: A cross-sectional study of HIV-1 infected adults with antiretroviral therapy for more than one year in the National Cheng Kung University Hospital was conducted.

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Background/aims: Restenosis after a percutaneous coronary intervention (PCI) during treatment for coronary artery disease is closely related to smooth muscle cell (SMC) proliferation and migration. In this study, we investigated the effects of caffeic acid phenethyl ester (CAPE) and its underlying mechanism on human coronary SMCs (HCSMCs) after platelet-derived growth factor-BB (PDGF-BB) stimulation in vitro.

Methods And Results: The results showed that CAPE inhibited proliferation and migration, and induced apoptosis.

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