Our aim was to analyze the association of HSPA1B genotypes and treatment response measured by the changes of psychopathology and neurocognitive symptoms in patients with first-episode psychosis (FEP) after 18 months of treatment. A sample of 159 patients with FEP admitted at two Croatian psychiatric hospitals in the period between year 2014 and year 2017 was assessed at baseline and after 18 months of follow-up with Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale for Schizophrenia (CDSS) and a battery of neurocognitive tests. Associations of scale and test results with HSPA1B polymorphic locus rs1061581 were analyzed using the general linear model. The carriers of the AA genotype showed the highest improvement in CDSS and RAVLT A test after the 18-month follow-up. Concordantly, we found significantly higher improvement assessed with the CDSS, RAVLT A, RAVLT A 30' and positive PANSS scales in the not-GG (AA/AG) group compared with the GG group. Our study suggests that HSPA1B rs1061581variants may moderate treatment response in FEP measured with changes of psychopathology and neurocognitive test results.
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http://dx.doi.org/10.1038/s41397-020-0150-9 | DOI Listing |
Cancers (Basel)
December 2024
CeRePP, 75020 Paris, France.
Purpose: To identify molecular changes during PCa invasion of adipose space using Spatial Transcriptomic Profiling of PCa cells.
Methods: This study was performed on paired intraprostatic and extraprostatic samples obtained from radical prostatectomy with pT3a pathological stages.
Results: Differential gene expression revealed upregulation of heat shock protein genes: DNAJB1, HSPA8, HSP90AA1, HSPA1B, HSPA1A in PCa PanCK+ cells from the adipose periprostatic space.
Int J Mol Sci
January 2025
Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 20201, USA.
Brain ischemia causes disruption in cerebral blood flow and blood-brain barrier integrity, which are normally maintained by astrocyte endfeet. Emerging evidence points to dysregulation of the astrocyte translatome during ischemia, but its effects on the endfoot translatome are unknown. In this study, we aimed to investigate the early effects of ischemia on the astrocyte endfoot translatome in a rodent cerebral ischemia and reperfusion model of stroke.
View Article and Find Full Text PDFJ Am Heart Assoc
January 2025
Department of Cardiology, Pulmonology, and Nephrology Yamagata University School of Medicine Yamagata Japan.
Background: Doxorubicin-induced cardiotoxicity is still an important medical problem associated with a high mortality rate in cancer survivors. p53 plays a key role in doxorubicin-induced cardiotoxicity. Diacylglycerol kinase ζ (Dgkζ), a 130-kDa enzyme abundant in cardiomyocytes, regulates the p53 protein expression level in neurons.
View Article and Find Full Text PDFDiscov Oncol
December 2024
Laboratory of Hematology-Oncology, European Institute of Oncology IRCCS, Via Ripamonti 435, 20141, Milan, MI, Italy.
The clinical presentation of T-cell large granular lymphocytic leukemia (T-LGLL) is extremely variable: 30% of patients have neutropenia with no associated symptoms, others present with bacterial infections and sepsis may occur. Tools to predict patient outcome are lacking. Stemming from preliminary results obtained by single cell-RNAseq we investigated by qPCR HSP and IFIT gene families in 27 LGLL patients (23T-LGLL and 4 NK-LGLL), including 11 with neutropenia and/or thrombocytopenia and 16 asymptomatic for the disease.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Department of Nephrology, Yi Ji Shan hospital affiliated to Wan Nan Medical college, Wuhu, Anhui, China.
Macrophages are recognized as vital players in renal fibrosis, with a high degree of heterogeneity and plasticity, and the triggering receptor expressed on myeloid cell-2 (TREM-2) is highly expressed on macrophages and participates in the progression of tissue fibrosis. However, the mechanism by which TREM-2 mediates the progression of renal fibrosis is still unclear. Our study revealed that exosomes derived from TREM-2-deficient (TREM-2) macrophages suppressed the progression of fibrosis, as indicated by a greater matrix metalloproteinase-9 (MMP-9)/tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) ratio at the protein level in secreted exosomes than in exosomes from wild-type (WT) macrophages in the fibrotic microenvironment.
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