The experimental visualisation of molecular structural changes during both photochemical and thermal reactions by real-time vibrational spectroscopy

2011 ◽  
Vol 13 (13) ◽  
pp. 5546 ◽  
Author(s):  
Izumi Iwakura
Pharmaceutics ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1485
Author(s):  
Aina Venkatasamy ◽  
Eric Guerin ◽  
Anais Blanchet ◽  
Christophe Orvain ◽  
Véronique Devignot ◽  
...  

The reasons behind the poor efficacy of transition metal-based chemotherapies (e.g., cisplatin) or targeted therapies (e.g., histone deacetylase inhibitors, HDACi) on gastric cancer (GC) remain elusive and recent studies suggested that the tumor microenvironment could contribute to the resistance. Hence, our objective was to gain information on the impact of cisplatin and the pan-HDACi SAHA (suberanilohydroxamic acid) on the tumor substructure and microenvironment of GC, by establishing patient-derived xenografts of GC and a combination of ultrasound, immunohistochemistry, and transcriptomics to analyze. The tumors responded partially to SAHA and cisplatin. An ultrasound gave more accurate tumor measures than a caliper. Importantly, an ultrasound allowed a noninvasive real-time access to the tumor substructure, showing differences between cisplatin and SAHA. These differences were confirmed by immunohistochemistry and transcriptomic analyses of the tumor microenvironment, identifying specific cell type signatures and transcription factor activation. For instance, cisplatin induced an “epithelial cell like” signature while SAHA favored a “mesenchymal cell like” one. Altogether, an ultrasound allowed a precise follow-up of the tumor progression while enabling a noninvasive real-time access to the tumor substructure. Combined with transcriptomics, our results underline the different intra-tumoral structural changes caused by both drugs that impact differently on the tumor microenvironment.


2019 ◽  
Vol 55 (4) ◽  
pp. 541-544 ◽  
Author(s):  
Shuji Ye ◽  
Junjun Tan ◽  
Kangzhen Tian ◽  
Chuanzhao Li ◽  
Jiahui Zhang ◽  
...  

Coherent degenerate infrared-infrared-visible sum frequency generation vibrational spectroscopy provides a powerful label-free probe for identifying the vibrational modes that are coupled through the electronic states in situ and in real time.


2019 ◽  
Vol 9 (6) ◽  
pp. 839-844
Author(s):  
Shuai Zhang ◽  
Weiwei Guo ◽  
Xin Zhao ◽  
Peng Li

Osteoporosis (OP) is a bone disease caused by various causes and can be found in various stages, such as juvenile, adult, menopausal and old age. OP has the systemic, degenerative, and metabolic characteristics, which leads to loss of bone mass, structural changes, and biomechanical properties degeneration. Prdx2 is a member of the peroxiredoxase family with antioxidant effects and involved in the regulation of bone and joint diseases. However, the role of Prdx2 in OP and related mechanisms has not been elucidated. SD rats were randomly divided into 2 groups, OP group in which OP rat model was prepared by ovariectomy and sham operation group. Prdx2 siRNA was transfected into OP rats followed by analysis of the expression of Prdx2, Opn, and Osterix by real-time PCR, bone density changes by dual energy line bone densitometer, formation of mineralized nodules by Alizarin red staining, Serum osteocalcin (OC) activity by ELISA as well as RANK and osteoprotegerin (OPG) expressions by real-time PCR and Western blot. Prdx2 expression was significantly increased, bone mineral density (BMD) was reduced, mineralized nodule formation was attenuated, Opn and Osterix levels were downregulated, together with decreased serum OC activity, increased RANK expression, and declined OPG expression apparently in OP rats compared with sham group (P < 0.05). Prdx2 siRNA transfection downregulated Prdx2 and RANK levels, increased BMD, mineralized nodule formation, Opn, OPG, and Osterix levels, as well as serum OC activity in OP rats (P < 0.05). Prdx2 expression is elevated in osteoporotic rats, which is associated with decreased osteogenic differentiation and BMD, leading to osteoporosis. Downregulation of Prdx2 expression can improve osteoporosis by regulating the RANK/OPG pathway.


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