Protection effect of sanguinarine on whole-body exposure of X radiation in BALB/c mice

To investigate the effects of sanguinarine (SAN) on acute radiation induced injury in mice, 45 mice were randomly divided into control, 10 Gy and SAN+10 Gy groups. Mice in the 10 Gy and SAN+10 Gy groups were exposed to single X-ray radiation with an accumulated dose of 10 Gy. Mice in the SAN+10 Gy group were administered intraperitoneally with 2.5 mg/kg body weight of SAN before radiation. Five days after radiation exposure, 5 mice from each group were sacrificed and samples of the small intestine, lung, spleen and liver were fixed for histopathological examinations. Compared with the 10 Gy group, radiation sickness was obviously delayed or attenuated in the SAN+10 Gy group. Survival analysis showed a significant difference between 2 radiation groups (PPara investigar os efeitos da sanguinarina (SAN) em lesões induzidas em ratos por radiação aguda, 45 ratos foram aleatoriamente divididos em grupo controle, grupo 10 Gy e grupo SAN+10 Gy. Os ratos dos grupos 10 Gy e SAN+10 Gy foram expostos à radiação de raio-X simples com uma dose acumulada de 10 Gy. Aos ratos do grupo SAN+10 Gy administraram-se, intraperitonealmente, 2.5 mg/kg de peso de SAN antes da radiação. Aos 5 dias de exposição à radiação, sacrificaram-se 5 ratos de cada grupo e retiraram-se amostras do intestino delgado, pulmões, baço e fígado para exames histopatológicos. Comparando com o grupo 10 Gy, a doença por radiação foi claramente atrasada e atenuada no grupo SAN+10 Gy. A análise de sobrevivência mostrou diferença significativa entre os dois grupos de radiação (

Prospective study of AI-assisted prediction of breast malignancies in physical health examinations: role of off-the-shelf AI software and comparison to radiologist performance

ObjectiveIn physical health examinations, breast sonography is a commonly used imaging method, but it can lead to repeated exams and unnecessary biopsy due to discrepancies among radiologists and health centers. This study explores the role of off-the-shelf artificial intelligence (AI) software in assisting radiologists to classify incidentally found breast masses in two health centers.MethodsFemale patients undergoing breast ultrasound examinations with incidentally discovered breast masses were categorized according to the 5th edition of the Breast Imaging Reporting and Data System (BI-RADS), with categories 3 to 5 included in this study. The examinations were conducted at two municipal health centers from May 2021 to May 2023.The final pathological results from surgical resection or biopsy served as the gold standard for comparison. Ultrasonographic images were obtained in longitudinal and transverse sections, and two junior radiologists and one senior radiologist independently assessed the images without knowing the pathological findings. The BI-RADS classification was adjusted following AI assistance, and diagnostic performance was compared using receiver operating characteristic curves.ResultsA total of 196 patients with 202 breast masses were included in the study, with pathological results confirming 107 benign and 95 malignant masses. The receiver operating characteristic curve showed that experienced breast radiologists had higher diagnostic performance in BI-RADS classification than junior radiologists, similar to AI classification (AUC = 0.936, 0.806, 0.896, and 0.950, p < 0.05). The AI software improved the accuracy, sensitivity, and negative predictive value of the adjusted BI-RADS classification for the junior radiologists’ group (p< 0.05), while no difference was observed in the senior radiologist group. Furthermore, AI increased the negative predictive value for BI-RADS 4a masses and the positive predictive value for 4b masses among radiologists (p < 0.05). AI enhances the sensitivity of invasive breast cancer detection more effectively than ductal carcinoma in situ and rare subtypes of breast cancer.ConclusionsThe AI software enhances diagnostic efficiency for breast masses, reducing the performance gap between junior and senior radiologists, particularly for BI-RADS 4a and 4b masses. This improvement reduces unnecessary repeat examinations and biopsies, optimizing medical resource utilization and enhancing overall diagnostic effectiveness

The Epigenetic Modifier PRDM5 Functions as a Tumor Suppressor through Modulating WNT/β-Catenin Signaling and Is Frequently Silenced in Multiple Tumors

BACKGROUND: PRDM (PRDI-BF1 and RIZ domain containing) proteins are zinc finger proteins involved in multiple cellular regulations by acting as epigenetic modifiers. We studied a recently identified PRDM member PRDM5 for its epigenetic abnormality and tumor suppressive functions in multiple tumorigeneses. METHODOLOGY/PRINCIPAL FINDINGS: Semi-quantitative RT-PCR showed that PRDM5 was broadly expressed in human normal tissues, but frequently silenced or downregulated in multiple carcinoma cell lines due to promoter CpG methylation, including 80% (4/5) nasopharyngeal, 44% (8/18) esophageal, 76% (13/17) gastric, 50% (2/4) cervical, and 25% (3/12) hepatocellular carcinoma cell lines, but not in any immortalized normal epithelial cell lines. PRDM5 expression could be restored by 5-aza-2'-deoxycytidine demethylation treatment in silenced cell lines. PRDM5 methylation was frequently detected by methylation-specific PCR (MSP) in multiple primary tumors, including 93% (43/46) nasopharyngeal, 58% (25/43) esophageal, 88% (37/42) gastric and 63% (29/46) hepatocellular tumors. PRDM5 was further found a stress-responsive gene, but its response was impaired when the promoter was methylated. Ectopic PRDM5 expression significantly inhibited tumor cell clonogenicity, accompanied by the inhibition of TCF/β-catenin-dependent transcription and downregulation of CDK4, TWIST1 and MDM2 oncogenes, while knocking down of PRDM5 expression lead to increased cell proliferation. ChIP assay showed that PRDM5 bound to its target gene promoters and suppressed their transcription. An inverse correlation between the expression of PRDM5 and activated β-catenin was also observed in cell lines. CONCLUSIONS/SIGNIFICANCE: PRDM5 functions as a tumor suppressor at least partially through antagonizing aberrant WNT/β-catenin signaling and oncogene expression. Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker

Differential Regulation of H3K9/H3K14 Acetylation by Small Molecules Drives Neuron-Fate-Induction of Glioma Cell

Differentiation therapy using small molecules is a promising strategy for improving the prognosis of glioblastoma (GBM). Histone acetylation plays an important role in cell fate determination. Nevertheless, whether histone acetylation in specific sites determines GBM cells fate remains to be explored. Through screening from a 349 small molecule-library, we identified that histone deacetylase inhibitor (HDACi) MS-275 synergized with 8-CPT-cAMP was able to transdifferentiate U87MG GBM cells into neuron-like cells, which were characterized by cell cycle arrest, rich neuron biomarkers, and typical neuron electrophysiology. Intriguingly, acetylation tags of histone 3 at lysine 9 (H3K9ac) were decreased in the promoter of multiple oncogenes and cell cycle genes, while ones of H3K9ac and histone 3 at lysine 14 (H3K14ac) were increased in the promoter of neuron-specific genes. We then compiled a list of genes controlled by H3K9ac and H3K14ac, and proved that it is a good predictive power for pathologic grading and survival prediction. Moreover, cAMP agonist combined with HDACi also induced glioma stem cells (GSCs) to differentiate into neuron-like cells through the regulation of H3K9ac/K14ac, indicating that combined induction has the potential for recurrence-preventive application. Furthermore, the combination of cAMP activator plus HDACi significantly repressed the tumor growth in a subcutaneous GSC-derived tumor model, and temozolomide cooperated with the differentiation-inducing combination to prolong the survival in an orthotopic GSC-derived tumor model. These findings highlight epigenetic reprogramming through H3K9ac and H3K14ac as a novel approach for driving neuron-fate-induction of GBM cells

A spectral data release for 104 Type II Supernovae from the Tsinghua Supernova Group

We present 206 unpublished optical spectra of 104 type II supernovae obtained by the Xinglong 2.16m telescope and Lijiang 2.4m telescope during the period from 2011 to 2018, spanning the phases from about 1 to 200 days after the SN explosion. The spectral line identifications, evolution of line velocities and pseudo equivalent widths, as well as correlations between some important spectral parameters are presented. Our sample displays a large range in expansion velocities. For instance, the Fe~{\sc ii} $5169$ velocities measured from spectra at $t\sim 50$ days after the explosion vary from ${\rm 2000\ km\ s^{-1}}$to${\rm 5500\ km\ s^{-1}}$, with an average value of${\rm 3872 \pm 949\ km\ s^{-1}}$. Power-law functions can be used to fit the velocity evolution, with the power-law exponent quantifying the velocity decline rate. We found an anticorrelation existing between H$\beta$velocity at mid-plateau phase and its velocity decay exponent, SNe II with higher velocities tending to have smaller velocity decay rate. Moreover, we noticed that the velocity decay rate inferred from the Balmer lines (i.e., H$\alpha$and H$\beta$) have moderate correlations with the ratio of absorption to emission for H$\alpha$ (a/e). In our sample, two objects show possibly flash-ionized features at early phases. Besides, we noticed that multiple high-velocity components may exist on the blue side of hydrogen lines of SN 2013ab, possibly suggesting that these features arise from complex line forming region. All our spectra can be found in WISeREP and Zenodo