Dysregulation of Angiogenesis and Inflammatory Genes in Endometrial Mesenchymal Stem Cells and Their Contribution to Endometriosis
Shermineh Heydari; Ladan Kashani; Mehrdad Noruzinia · 2021 · Iranian Journal of Allergy, Asthma and Immunology
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Endometriosis is a common, chronic, inflammatory disorder in women, characterized by the presence of endometrial tissue outside the uterus cavity. The disease affects ~10% of women during their reproductive age. There is some debates on the pathogenesis of endometriosis and its mechanism among the scientists; therefore, different hypotheses have been suggested. According to Sampson theory, a possible mechanism for seeding ectopic endometriotic lesions is a dysregulation of endometrial mesenchymal stem cells (eMSCs). In the present study, we evaluated the expression of candidate genes in eMSCs
Abstract by Shermineh Heydari; Ladan Kashani; Mehrdad Noruzinia, Iranian Journal of Allergy, Asthma and Immunology (2021) — licensed CC BY 4.0.
About to run something similar?
Run an AI Precheck on your own design to catch failure modes like this one before you spend the time. Your first desk check is free.
Related failures
A Randomized Trial of Intraarterial Treatment for Acute Ischemic Stroke
Negative / Null Result ReportDuodenal Infusion of Donor Feces for Recurrent Clostridium difficile
Negative / Null Result ReportStenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis
Negative / Null Result ReportEffects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
Replication FailureA Randomized Trial of Bevacizumab for Newly Diagnosed Glioblastoma
Negative / Null Result ReportSpironolactone for Heart Failure with Preserved Ejection Fraction
WASTE indexes this work — it does not host or republish it. Failure-type classification is automated and approximate.
Metadata source: DOAJ