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Balkan Journal of Medical Genetics :... May 2023The term "aristolochic acid nephropathy" (AAN) is used to include any form of toxic interstitial nephropathy that is caused either by ingestion of plants containing...
Molecular Characterization of Microrna Interference and Aristolochic Acid Intoxication Found in Upper Tract Urothelial Carcinoma in Patients with Balkan Endemic Nephropathy: A Systematic Review of the Current Literature.
The term "aristolochic acid nephropathy" (AAN) is used to include any form of toxic interstitial nephropathy that is caused either by ingestion of plants containing aristolochic acids (AA) or by the environmental contaminants in food such as in Balkan endemic nephropathy (BEN). Aristolochic acid (AA) intoxication is strongly associated with the development of upper tract urothelial carcinoma (UTUC); however, the underlying molecular mechanism remains to be defined. MicroRNAs (miRNA) regulate several biological processes, including cell proliferation, differentiation, and metabolism, acting as oncogenes or tumor suppressors. A unique miRNA expression profile suggested that miRNAs could function as regulators in UTUC developmental processes. This review aimed to summarize data available in the literature about underlying molecular mechanisms leading to the expression of miRNAs in AA-UTUC patients with BEN. Strong correlation in AA-UTUC has a distinctive gene alteration pattern, AL-DNA adducts, and a unique tumor protein (TP53) mutational spectrum AAG to TAG (A: T→T: A) transversion in codon 139 (Lys → Stop) of exon 5 activates the p53 tumor suppressor protein. Further, p53 protein is responsible not only for the expression of miRNAs but also acts as a target molecule for miRNAs and plays a crucial function in the AA-UTUC pathogenicity through activation of cyclin-dependent kinase (CyclinD1) and cyclin protein kinase 6(CDK6) to support cell cycle arrest. This study, proposed a molecular mechanism that represented a possible unique relationship between AA intoxication, miRNAs expression, and the progression of UTUC in patients with BEN.
PubMed: 37265966
DOI: 10.2478/bjmg-2022-0027 -
Acta Obstetricia Et Gynecologica... Jan 2011The terrorist explosions of the World Trade Center in New York City and the other events on the Pentagon and in Pennsylvania on 11 September 2001 were stressful events...
BACKGROUND
The terrorist explosions of the World Trade Center in New York City and the other events on the Pentagon and in Pennsylvania on 11 September 2001 were stressful events that affected people around the world. Pregnant women and their offspring are especially vulnerable during and after such a terrorist attack. The objective was to systematically review the risks of adverse pregnancy outcomes after the terrorist attacks on Sept 11, 2001.
METHODS
The Meta-analysis of Observational Studies in Epidemiology (MOOSE) criteria were used for reporting of this review. Statistical analyses were performed using RevMan 5.0.
RESULTS
Ten reports of low-to-moderate risk of methodological bias were included. There was increased risks of infants with birthweight of 1,500 g-1,999 g (adjusted odds ratio [AOR] 1.67 [95%CI 1.11-2.52]) and small-for-gestational age births (AOR 1.90; 95%CI 1.05-3.46) in New York. There was increased risks of low birthweight (relative risk 2.25; 95%CI 1.29-3.90) and preterm births (relative risk 1.50; 95%CI 1.06-2.14) among ethnically Arabic women living in California There was a reduction in birthweight by 276 g and in head circumference by 1 cm when DNA adducts, a marker for environmental toxin exposure, were doubled in maternal blood. In Holland, a 48-g reduction in birthweight was reported.
CONCLUSIONS
The World Trade Center disaster influenced pregnancy outcomes in New York, among ethnically Arab women living in California and among Dutch women. The adverse outcomes are likely due to environmental pollution and stress in New York, ethnic harassment in California and communal bereavement and stress in Holland.
Topics: Female; Humans; Pregnancy; Pregnancy Complications; September 11 Terrorist Attacks
PubMed: 21275910
DOI: 10.1111/j.1600-0412.2010.01020.x