Do periodontal defects affect periodontal inflammation and destruction? ‐Histological/microbiological changes and gene expression profiles of a pilot study in beagle dogs

Author(s):  
Yin‐Zhe An ◽  
Kyung‐A Ko ◽  
Chang‐Sung Kim ◽  
Reinhard Gruber ◽  
Xinhong Wang ◽  
...  
Gut ◽  
2021 ◽  
pp. gutjnl-2021-326552
Author(s):  
Andrea C Masi ◽  
Tatiana Y Fofanova ◽  
Christopher A Lamb ◽  
Jennifer M Auchtung ◽  
Robert A Britton ◽  
...  

Author(s):  
Petra Stute ◽  
S. Ehrentraut ◽  
H.-H. Henneicke-von Zepelin ◽  
P. Nicken

Abstract Purpose This study aimed at assessing gene expression profiles in hippocampus and hypothalamus of ovariectomized (OVX) rats with or without treatment with an isopropanolic extract of Cimicifuga racemosa rhizomes (iCR) in comparison to intact rats. Methods Exploration of hippocampal (Hi) and hypothalamic (Hy) tissue from Sprague Dawley rats: without OVX (NHi = NHy = 4), tissues 3 months after OVX (NHi = 4, NHy = 3), or tissues of rats after their treatment with iCR for 3 months after OVX (NHi = NHy = 2). Gene expression profiles in these tissues were investigated by RNA-microarray-analysis and subsequent verification by qPCR. Results 4812 genes were differentially regulated when comparing the three groups in hippocampus and hypothalamus. iCR compensated the effects of OVX in 518 genes. This compensatory effect was most prominent in hippocampal signalling pathways, thereof genes (GAL, CALCA, HCRT, AVPR1A, PNOC, etc.) involved in thermoregulation, regulation of sleep and arousal, blood pressure regulation, metabolism, nociception, hormonal regulation, homeostasis, learning and cognition, mood regulation, neuroendocrine modulation, etc.. In the hypothalamus, iCR compensated OVX-effects at TAC3 and OPRM1 but not at KISS1. These genes are involved in the pathophysiology of hot flashes. Conclusions Our pilot study findings support a multifaceted mode of action of iCR in menopausal complaints on a tissue-specific brain gene expression level.


2022 ◽  
Vol 18 (1) ◽  
Author(s):  
Chiao-Hsu Ke ◽  
Hirotaka Tomiyasu ◽  
Yu-Ling Lin ◽  
Wei-Hsiang Huang ◽  
Hsiao-Hsuan Huang ◽  
...  

Abstract Background Canine transmissible venereal tumours (CTVTs) can cross the major histocompatibility complex barrier to spread among dogs. In addition to the transmissibility within canids, CTVTs are also known as a suitable model for investigating the tumour–host immunity interaction because dogs live with humans and experience the same environmental risk factors for tumourigenesis. Moreover, outbred dogs are more appropriate than inbred mice models for simulating the diversity of human cancer development. This study built a new model of CTVTs, known as MCTVTs, to further probe the shaping effects of immune stress on tumour development. For xenotransplantation, CTVTs were first injected and developed in immunodeficient mice (NOD.CB17-Prkdcscid/NcrCrl), defined as XCTVTs. The XCTVTs harvested from NOD/SCID mice were then inoculated and grown in beagles and named mouse xenotransplantation of CTVTs (MCTVTs). Results After the inoculation of CTVTs and MCTVTs into immune-competent beagle dogs separately, MCTVTs grew faster and metastasized more frequently than CTVTs did. Gene expression profiles in CTVTs and MCTVTs were analysed by cDNA microarray to reveal that MCTVTs expressed many tumour-promoting genes involved in chronic inflammation, chemotaxis, extracellular space modification, NF-kappa B pathways, and focal adhesion. Furthermore, several well-known tumour-associated biomarkers which could predict tumour progression were overexpressed in MCTVTs. Conclusions This study demonstrated that defective host immunity can result in gene instability and enable transcriptome reprogramming within tumour cells. Fast tumour growth in beagle dogs and overexpression of tumour-associated biomarkers were found in a CTVT strain previously established in immunodeficient mice. In addition, dysregulated interaction of chronic inflammation, chemotaxis, and extracellular space modification were revealed to imply the possibly exacerbating mechanisms in the microenvironments of these tumours. In summary, this study offers a potential method to facilitate tumour progression and provide a niche for discovering tumour-associated biomarkers in cancer research.


2017 ◽  
Vol 40 ◽  
pp. e10
Author(s):  
A. Alisi ◽  
R. Brugaletta ◽  
A.P. Santoro ◽  
N. Panera ◽  
G. Dalmasso ◽  
...  

Biomarkers ◽  
2003 ◽  
Vol 8 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Laurie A. Davidson ◽  
Joanne R. Lupton ◽  
Emil Miskovsky ◽  
Alan P. Fields ◽  
Robert S. Chapkin

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