scholarly journals Effects of long-term treatment with pioglitazone on cognition and glucose metabolism of PS1-KI, 3xTg-AD, and wild-type mice

2012 ◽  
Vol 3 (12) ◽  
pp. e448-e448 ◽  
Author(s):  
F Masciopinto ◽  
N Di Pietro ◽  
C Corona ◽  
M Bomba ◽  
C Pipino ◽  
...  
2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Saif Khan ◽  
Raju K. Mandal ◽  
Abdulbaset Mohamed Elasbali ◽  
Sajad A. Dar ◽  
Arshad Jawed ◽  
...  

Abstract Hepatotoxicity is a severe problem generally faced by tuberculosis (TB) patients. It is a well-known adverse reaction due to anti-TB drugs in TB patients undergoing long-term treatment. The studies published previously have explored the connection of N-acetyltransferase 2 (NAT2) gene polymorphisms with isoniazid-induced hepatotoxicity, but the results obtained were inconsistent and inconclusive. A comprehensive trial sequence meta-analysis was conducted employing 12 studies comprising 3613 controls and 933 confirmed TB cases using the databases namely, EMBASE, PubMed (Medline) and Google Scholar till December 2017. A significant association was observed with individuals carrying variant allele at position 481C>T (T vs. C: P = 0.001; OR = 1.278, 95% CI = 1.1100–1.484), at position 590G>A (A vs. G: P = 0.002; OR = 1.421, 95% CI = 1.137–1.776) and at position 857G>A (A vs. G: P = 0.0022; OR = 1.411, 95% CI = 1.052–1.894) to higher risk of hepatotoxicity vis-à-vis wild-type allele. Likewise, the other genetic models of NAT2 gene polymorphisms have also shown increased risk of hepatotoxicity. No evidence of publication bias was observed. These results suggest that genetic variants of NAT2 gene have significant role in isoniazid induced hepatotoxicity. Thus, NAT2 genotyping has the potential to improve the understanding of the drug–enzyme metabolic capacity and help in early predisposition of isoniazid-induced hepatotoxicity.


1992 ◽  
Vol 43 (1) ◽  
pp. 47-50 ◽  
Author(s):  
A. Bruno ◽  
G. Pagano ◽  
L. Benzi ◽  
G. Di Ciani ◽  
V. Spallone ◽  
...  

2009 ◽  
Vol 618 (1-3) ◽  
pp. 98-104 ◽  
Author(s):  
Kenji Katsuno ◽  
Yoshikazu Fujimori ◽  
Yukiko Ishikawa-Takemura ◽  
Masayuki Isaji

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yilang Li ◽  
Yunpei Mai ◽  
Xiaoxia Qiu ◽  
Xiaoqing Chen ◽  
Conglin Li ◽  
...  

2001 ◽  
Vol 361 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Nino MZHAVIA ◽  
Yimei QIAN ◽  
Yun FENG ◽  
Fa-Yun CHE ◽  
Lakshmi A. DEVI ◽  
...  

ProSAAS, a recently discovered granin-like protein, potently inhibits prohormone convertase (PC)1, and might also perform additional functions. In the present study, the processing of proSAAS was compared in two neuroendocrine cell lines overexpressing this protein: the AtT-20 mouse pituitary corticotrophic line and the PC12 rat adrenal phaeochromocytoma line. The processing of proSAAS was examined by pulse–chase analysis using [3H]leucine, by MS, and by chromatography and radioimmunoassay. Various smaller forms of proSAAS were detected, including peptides designated as little SAAS, PEN and big LEN. Because the PC-12 cells used in the present study do not express either PC1 or PC2, the finding that these cells efficiently cleave proSAAS indicates that these cleavages do not require either enzyme. Two of the peptides identified in AtT-20 media represent novel C-terminally truncated forms of PEN. In both cell lines, the secretion of the small proSAAS-derived peptides is stimulated by secretagogues. However, long-term treatment of wild-type AtT-20 cells with two different secretagogues (8-bromo-cAMP and a phorbol ester) does not affect levels of proSAAS mRNA; this treatment significantly increases PC1 mRNA by approx. 60–80%. The lack of co-regulation of proSAAS and PC1 mRNA implies that enzyme activity can be induced without an accompanying increase in the inhibitor. In addition, the finding that the peptides are secreted via the regulated pathway is consistent with the proposal that they may function as neuropeptides.


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