RESUMO
Robust preclinical models are inevitable for researchers to unravel pathomechanisms of subarachnoidal hemorrhage (SAH). For the mouse perforation model of SAH, the goal of this meta-review was the determination of variances in mortality, SAH severity grade, and vasospasm, and their experimental moderators, as many researchers are facing with incomparable results. We searched on the databases PubMed, Embase, and Web of Science for articles describing in vivo experiments using the SAH perforation mouse model and measuring mortality, SAH grade, and/or vasospasm. After screening, 42 articles (total of 1964 mice) were included into systematic review and meta-analysis. Certain model characteristics were insufficiently reported, e.g., perforation location (not reported in six articles), filament (material (n = 15) and tip texture (n = 25)), mouse age (n = 14), and weight (n = 10). Used injective anesthetics and location of perforation showed large variation. In a random-effects meta-analysis, the overall animal mortality following SAH was 21.3% [95% CI: 17.5%, 25.7%] and increased with longer observational periods. Filament material significantly correlated with animal mortality (p = 0.024) after exclusion of hyperacute studies (time after SAH induction < 24 h). Reported mean SAH grade was 10.7 [9.6, 11.7] on the scale of Sugawara (J Neurosci Methods 167:327-34, 2008). Furthermore, mean diameter of large cerebral arteries after SAH was reduced by 27.6% compared to sham-operated non-SAH mice. Uniforming standards of experimental procedures and their reporting are indispensable to increase overall comparability.
RESUMO
Background: Acrosin binding protein (ACRBP) is a member of the cancer-testis antigen (CTA) family. Normally, ACRBP mRNA is expressed only in seminiferous tubules, while abnormally it is expressed in various types of cancers in tumor tissues, such as brain tumor. Objectives: To determine the expression and clinical impact of a newly discovered splice variant of ACRBP in brain tumor. Methods: Total RNA was extracted and reverse transcribed from 92 tumor specimens and 3 cell lines. Primers were designed to determine the expression of the new splice variant in all the samples. Quantitative real-time PCR (qPCR) was conducted for samples positive in reverse transcriptase-PCR. Association of the expression of ACRBP with the clinicopathological features of the various brain tumors was assessed statistically. Results: The primers identified a newly discovered splice variant of ACRBP named ACRBP-V5a. The proportions of samples of the various brain tumor types positive for the ACRBP-V5a splicing variant were as follows: astrocytoma 10/33 (30%), glioblastoma 10/30 (33%), medulloblastoma 14/29 (48%), all tumors 34/92 (37%). Although we did not find a significant difference in the proportions of samples of various types of brain tumor tissues positive for the new splice variant (P > 0.05), levels of expression of the ACRBP-V5a splice variant were significantly different for tumor grade (P = 0.01) and tumor type (P = 0.02). Conclusions: A newly discovered splice variant, ACRBP-V5a, is present in brain tumor. The new splicing variant may have discriminative value and potential importance in molecular-targeted therapy for brain tumors.
