Towards disentangling the classification of freshwater fish trypanosomes

Currently, new species of freshwater fish trypanosomes, which are economically important parasites, are being described based on subjectively selected features, i.e., their cell morphology and the host species. We have performed detailed phylogenetic and haplotype diversity analyses of all 18S rRNA genes available for freshwater fish trypanosomes, including the newly obtained sequences of Trypanosoma carassii and Trypanosoma danilewskyi. Based on a sequence similarity of 99.5%, we divide these trypanosomes into 15 operational taxonomic units, and propose three nominal scenarios for distinguishing T. carassii and other aquatic trypanosomes. We find evidences for the existence of a low number of freshwater fish trypanosomes, with T. carassii having the widest geographic and host ranges. Our analyses support the existence of an umbrella complex composed of T. carassii and two sister species

An acquired phosphatidylinositol 4-phosphate transport initiates T-cell deterioration and leukemogenesis

Publisher Copyright: © 2022, The Author(s).Lipid remodeling is crucial for malignant cell transformation and tumorigenesis, but the precise molecular processes involved and direct evidences for these in vivo remain elusive. Here, we report that oxysterol-binding protein (OSBP)-related protein 4 L (ORP4L) is expressed in adult T-cell leukemia (ATL) cells but not normal T-cells. In ORP4L knock-in T-cells, ORP4L dimerizes with OSBP to control the shuttling of OSBP between the Golgi apparatus and the plasma membrane (PM) as an exchanger of phosphatidylinositol 4-phosphate [PI(4)P]/cholesterol. The PI(4)P arriving at the PM via this transport machinery replenishes phosphatidylinositol 4,5-bisphosphate [PI(4,5)P-2] and phosphatidylinositol (3,4,5) trisphosphate [PI(3,4,5)P-3] biosynthesis, thus contributing to PI3K/AKT hyperactivation and T-cell deterioration in vitro and in vivo. Disruption of ORP4L and OSBP dimerization disables PI(4)P transport and T-cell leukemogenesis. In summary, we identify a non-vesicular lipid transport machinery between Golgi and PM maintaining the oncogenic signaling competence initiating T-cell deterioration and leukemogenesis. The oxysterol-binding protein-related protein 4 (ORP4L) is expressed in T-cell acute lymphoblastic leukemia and is required for leukemogenesis. Here the authors show that ORP4L orchestrates the transport of the phospholipid PI(4)P from Golgi to the plasma membrane, contributing to PI3K/AKT hyperactivation and T-cell leukemogenesis.Peer reviewe

Clinical efficacy of robotic spine surgery: an updated systematic review of 20 randomized controlled trials

Purpose: To determine whether using robots in spine surgery results in more clinical advantages and fewer adverse consequences. Methods: Between October 1990 and October 2022, a computer-based search was conducted through the databases of PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure, China Biology Medicine, VIP databases, and WAN FANG. The study only included randomized controlled trials (RCTs) comparing the clinical efficacy and safety of robot-assisted surgery with those of conventional spine surgery. The review was conducted following PRISMA 2020, and AMSTAR-2 was used to evaluate the methodological quality. R version 4.2.1 was used in the meta-analysis. The Cochrane Collaboration Tool was used for evaluating the risk of bias. Results: This study analyzed 954 participants from 20 RCTs involving cervical spondylosis, lumbar degenerative disease, scoliosis, etc. The robot-assisted group outperformed the freehand group in terms of intraoperative blood loss, number of screws in grade A position, grade A + B position, radiation dose, and hospital stay. Operation duration, visual analog scale scores of low back pain, Oswestry disability index, and radiation exposure time did not significantly differ between the two groups. Conclusions: Although robotic spine surgery is more accurate in pedicle screw placement than conventional methods, the robot group did not demonstrate an advantage in terms of clinical efficacy. Studies of complications and cost-effectiveness are still very rare

Analysis of Genes Related to Angiotensin II-Induced Arterial Injury Using a Time Series Microarray

Background/Aims: Angiotensin II (Ang II)-mediated hypertension is a major risk factor for cardiovascular diseases. Ang II induces changes in vessel structure and function through the activation of genes related to signaling pathways. However, the changes in the gene expression profiles of blood vessels in response to Ang II remain unclear. Methods: Wild-type C57BL/6 mice were infused with Ang II (1500 ng/kg/min) using an osmotic pump for 1, 3, and 7 days. Vascular wall inflammation and remodeling were evaluated by pathological examination. Time-series microarray and quantitative PCR analyses were performed. Bioinformatics analyses were conducted to identify key genes, pathways, and biological processes. Results: After Ang II infusion, blood pressure and aortic remodeling were increased over time. Microarray analysis identified a totally of 3631 differentially expressed genes in aortas at days 1, 3, and 7 of Ang II infusion. These genes were involved in multiple biological processes, including cell adhesion, angiogenesis, cell migration, protein phosphorylation, immune system, and cell cycle, which may play important roles in regulating Ang II-induced arterial injury during hypertension. The genes were classified into 50 profiles by hierarchical cluster analysis, and finally, 14 significant profiles were identified. Among these genes, protein kinase cAMP-activated catalytic subunit alpha (Prkaca), a gene that directly regulated 137 neighboring genes, was located at the center of the gene network in Ang II-infused aortas. Further, Prkaca protein expression and cAMP level were downregulated in a time-dependent manner in Ang II-infused aortas. Conclusions: The combined use of DNA microarrays and cluster and gene network analyses identified Prkaca as a key Ang II-responsive gene that may mediate early vascular injury and hypertension