Ultrasound Viscosity Imaging in Breast Lesions: A Multicenter Prospective Study.

RATIONALE AND OBJECTIVES: To explore and validate the clinical value of ultrasound (US) viscosity imaging in differentiating breast lesions by combining with BI-RADS, and then comparing the diagnostic performances with BI-RADS alone. MATERIALS AND METHODS: This multicenter, prospective study enrolled participants with breast lesions from June 2021 to November 2022. A development cohort (DC) and validation cohort (VC) were established. Using histological results as reference standard, the viscosity-related parameter with the highest area under the receiver operating curve (AUC) was selected as the optimal one. Then the original BI-RADS would upgrade or not based on the value of this parameter. Finally, the results were validated in the VC and total cohorts. In the DC, VC and total cohorts, all breast lesions were divided into the large lesion, small lesion and overall groups respectively. RESULTS: A total of 639 participants (mean age, 46 years ± 14) with 639 breast lesions (372 benign and 267 malignant lesions) were finally enrolled in this study including 392 participants in the DC and 247 in the VC. In the DC, the optimal viscosity-related parameter in differentiating breast lesions was calculated to be A'-S2-Vmax, with the AUC of 0.88 (95% CI: 0.84, 0.91). Using > 9.97 Pa.s as the cutoff value, the BI-RADS was then modified. The AUC of modified BI-RADS significantly increased from 0.85 (95% CI: 0.81, 0.88) to 0.91 (95% CI: 0.87, 0.93), 0.85 (95% CI: 0.80, 0.89) to 0.90 (95% CI: 0.85, 0.93) and 0.85 (95% CI: 0.82, 0.87) to 0.90 (95% CI: 0.88, 0.92) in the DC, VC and total cohorts respectively (P < .05 for all). CONCLUSION: The quantitative viscous parameters evaluated by US viscosity imaging contribute to breast cancer diagnosis when combined with BI-RADS.

Oncostatin M promotes the ox-LDL-induced activation of NLRP3 inflammasomes via the NF-κB pathway in THP-1 macrophages and promotes the progression of atherosclerosis.

Background: Oncostatin M (OSM) is reported to be involved in many stages of atherosclerosis, including endothelial dysfunction, chronic inflammation, and smooth muscle cell migration. This study explored the effects of OSM on foam cell formation and its corresponding molecular mechanisms. Methods: THP-1 cells were treated with phorbol-12-myristate-13-acetate (PMA) to induce macrophage differentiation and were then exposed to oxidized low-density lipoprotein (ox-LDL). OSM expression was analyzed by quantitative reverse transcription-polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay (ELISA). OSM-specific small interfering RNAs (siRNAs) were transfected into THP-1 macrophages. The effects of OSM silencing were evaluated by Oil Red O staining, ELISA, and Western blotting. Moreover, the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasomes was detected by western blotting and immunofluorescence. Results: OSM was highly expressed in THP-1 macrophages in a time- and dose-dependent fashion. Silencing OSM significantly reduced the total cholesterol content and Oil Red O staining levels in ox-LDL-treated macrophages. Silencing OSM significantly inhibited ox-LDL-induced cytokine release, including TNF-α, IL-1ß, IL-6, and IL-18. Ox-LDL activated p65 and NLRP3, which further induced caspase-1 cleavage, apoptosis-associated, speck-like protein containing a caspase-1 recruitment domain (ASC) upregulation, and gasdermin-D (GSDMD)-N fragmentation. Overexpression of NLRP3 significantly reversed the effects of OSM silencing on ox-LDL-induced foam cell formation and inflammation. Conclusions: OSM was highly expressed in the cell model of atherosclerosis. OSM has a promoting role in ox-LDL-induced foam cell formation and inflammation via the activation of p65-NLRP3 signaling pathways. Silencing OSM may be has benefit in treating atherosclerosis.

Efficacy and safety of drug-coated balloon versus non-drug-coated balloon combined with bare metal stent implantation in treatment of patients with occlusions of the superficial femoral artery: a retrospective study in clinical practice.

OBJECTIVE: To assess the efficacy and safety of drug-coated balloon and non-drug-coated balloon combined with bare metal stent implantation for the treatment of patients with occlusions of the superficial femoral artery. METHODS: In this retrospective study, 83 patients with occlusions of the superficial femoral artery were included. Among them, 41 patients received paclitaxel drug coated balloon treatment combined with bare metal stent implantation treatment (experimental group), the remaining 42 received non-drug-coated balloon treatment (control group). Patients were followed up at 1, 6, and 12 months after surgery. The primary clinical assessments, including ankle brachial index (ABI), RutherFord grade, Doppler ultrasound, or CT angiography (CTA), were used to observe the patency of target vessels, perioperative and postoperative complications. RESULTS: All the diseased vessels were successfully opened. There were no serious intraoperative complications such as vascular rupture or acute thrombosis. There was no significant difference in ankle brachial index, RutherFord grade, and total score between the two groups at one month and six months after operation (P>0.05). There was no significant difference in mortality, amputation rate, or thrombosis between the two groups (P>0.05). Twelve months after the operation, the ankle brachial index, Rutherford grade and total score of the experimental group were better than those of the control group (P<0.05). There was no significant difference in mortality, amputation rate, or thrombosis between the two groups (P>0.05). CONCLUSION: Paclitaxel coated balloon is safe and effective in the treatment of superficial femoral arteriosclerosis occlusion. It can significantly improve the ABI and Rutherford grades of patients, and it had a higher patency rate and lower reconstruction rate, but it may affect the healing ability of foot ulcer.

Characterization of regulatory regions involved in the inducible expression of chiB in Bacillus thuringiensis.

Expression of the chiB gene from Bacillus thuringiensis Bti75 was defined as inducible by the use of transcriptional fusions with the bgaB reporter gene. The transcription start site of the chiB gene was identified as the C base located 132 base pairs upstream of the start codon. Analysis of 5' and 3' deletions of the chiB promoter region revealed that the sequence from position -192 to +36 with respect to the transcription start site was necessary for wild-type levels of inducible expression of the chiB gene. The minimal promoter region for the expression of chiB gene was identified as the sequence from position -100 to +12. Furthermore, a 16-bp sequence (designated dre) downstream of the minimal promoter region of chiB was shown to be required for chitin induction. To confirm the function of this 16-bp sequence, 25 base substitutions were introduced into the dre site. Most of the mutations resulted in constitutive expression, or the efficiency of induction decreased. All mutations identified the dre sequence as a critical site for the inducible expression of chiB. In addition, the dre site was shown to interact with a sequence-specific DNA binding factor of strain Bti75 cultured in the absence of the inducer.

[Regulation of chitinase genes expression in bacteria].

Chitinases, which can hydrolyze chitin, occur in a wide range of microorganisms including viruses, bacteria, and fungi. The derivatives of chitin are potentially useful in several areas such as food processing, medicines, and biological control in agriculture. Some bacteria can uptake and utilize chitin as carbon source by secreting chitinase. The chitin is degraded into chito-oligosaccharides [(GlcNAc)n] or N-acetylglucosamine (GlcNAc) by chitinases, and then the chitin derivatives are transferred into cells by specific transport systems of bacteria. The intracellular chitin derivatives activate or suppress the transcription of a series of chi genes and affect the amount of chitinase. The expression of chitinase genes are strictly regulated by various regulatory factors and responsive cis-acting elements. The present review will focus on the transport system and the regulation of chitinase genes expression in bacteria.