CLIP-Driven Prototype Network for Few-Shot Semantic Segmentation.

Recent research has shown that visual-text pretrained models perform well in traditional vision tasks. CLIP, as the most influential work, has garnered significant attention from researchers. Thanks to its excellent visual representation capabilities, many recent studies have used CLIP for pixel-level tasks. We explore the potential abilities of CLIP in the field of few-shot segmentation. The current mainstream approach is to utilize support and query features to generate class prototypes and then use the prototype features to match image features. We propose a new method that utilizes CLIP to extract text features for a specific class. These text features are then used as training samples to participate in the model's training process. The addition of text features enables model to extract features that contain richer semantic information, thus making it easier to capture potential class information. To better match the query image features, we also propose a new prototype generation method that incorporates multi-modal fusion features of text and images in the prototype generation process. Adaptive query prototypes were generated by combining foreground and background information from the images with the multi-modal support prototype, thereby allowing for a better matching of image features and improved segmentation accuracy. We provide a new perspective to the task of few-shot segmentation in multi-modal scenarios. Experiments demonstrate that our proposed method achieves excellent results on two common datasets, PASCAL-5i and COCO-20i.

Manipulating PML SUMOylation via Silencing UBC9 and RNF4 Regulates Cardiac Fibrosis.

The promyelocytic leukemia protein (PML) is essential in the assembly of dynamic subnuclear structures called PML nuclear bodies (PML-NBs), which are involved in regulating diverse cellular functions. However, the possibility of PML being involved in cardiac disease has not been examined. In mice undergoing transverse aortic constriction (TAC) and arsenic trioxide (ATO) injection, transforming growth factor ß1 (TGF-ß1) was upregulated along with dynamic alteration of PML SUMOylation. In cultured neonatal mouse cardiac fibroblasts (NMCFs), ATO, angiotensin II (Ang II), and fetal bovine serum (FBS) significantly triggered PML SUMOylation and the assembly of PML-NBs. Inhibition of SUMOylated PML by silencing UBC9, the unique SUMO E2-conjugating enzyme, reduced the development of cardiac fibrosis and partially improved cardiac function in TAC mice. In contrast, enhancing SUMOylated PML accumulation, by silencing RNF4, a poly-SUMO-specific E3 ubiquitin ligase, accelerated the induction of cardiac fibrosis and promoted cardiac function injury. PML colocalized with Pin1 (a positive regulator for TGF-ß1 mRNA expression in PML-NBs) and increased TGF-ß1 activity. These findings suggest that the UBC9/PML/RNF4 axis plays a critical role as an important SUMO pathway in cardiac fibrosis. Modulating the protein levels of the pathway provides an attractive therapeutic target for the treatment of cardiac fibrosis and heart failure.

Adverse Respiratory Events Increase Post-anesthesia Care Unit Stay in China: A 2-year Retrospective Matched Cohort Study.

Despite growing attention to patients' safety worldwide, no data were available on the impact of adverse respiratory events (AREs) on post-anesthesia care and post-operation care in China. This study evaluated the occurrence of AREs, the impact of AREs on length of stay (LOS) in post-anesthesia care unit (PACU) and postoperative time in hospital, and PACU cost and inpatient healthcare costs. A retrospective, matched-cohort study was conducted by prospectively collecting the data of 159 AREs in PACU during 2016-2017 in an university hospital in China. Records were reviewed by pre-trained, qualified nurses and/or anesthesiologists. The incidence and the impact of AREs were analyzed. The LOS in PACU and postoperative time in hospital and the costs in PACU and inpatient healthcare costs were also obtained. Results showed that there were 253 AREs involving 156 patients. Hypoxia (n=141, 55.73%) and respiratory depression (n=70, 27.67%) were the most common AREs. Measurement data including body mass index (BMI) (22.85±4.36 vs. 22.32±3.83), duration of procedure (138.47±77.33 min vs. 137.44±72.33 min), duration of anesthesia (176.35±82.66 min vs. 174.61±78.08 min), LOS (16.53±10.65 days vs. 16.57±9.56 days), inpatient healthcare costs ($9465.57±9416.33 vs. $8166.51±5762.01), and postoperative LOS (11.26±8.77 days vs. 11.19±8.30 days) showed no significant differences between ARE and matched groups (P>0.05). Duration (81.65±54.79 min vs. 38.89±26.09 min) and costs ($31.99±17.80 vs. $18.72±8.39) in PACU were significantly different in ARE group from those in matched group (P<0.001). Proportion of patients with prolonged stay in PACU was significantly higher in ARE group than in matched group (18.59% vs. 1.28%), with an odds ratio (after matching) of 17.58 (95% CI=4.11 to 75.10; P<0.001). The AREs that occurred during the immediate postoperative period in PACU increased the incidence rate of prolonged stay, delayed the PACU stay, and increased the costs in PACU, resulting in the need of higher levels of postoperative care than anticipated, but the postoperative LOS and inpatient healthcare costs were unchanged.

Arsenic trioxide and angiotensin II have inhibitory effects on HERG protein expression: Evidence for the role of PML SUMOylation.

The human ether-a-go-go-related gene (HERG) channel is a novel target for the treatment of drug-induced long QT syndrome, which causes lethal cardiotoxicity. This study is designed to explore the possible role of PML SUMOylation and its associated nuclear bodies (NBs) in the regulation of HERG protein expression. Both arsenic trioxide (ATO) and angiotensin II (Ang II) were able to significantly reduce HERG protein expression, while also increasing PML SUMOylation and accelerating the formation of PML-NBs. Pre-exposure of cardiomyocytes to a SUMOylation chemical inhibitor, ginkgolic acid, or the silencing of UBC9 suppressed PML SUMOylation, subsequently preventing the downregulation of HERG induced by ATO or Ang II. Conversely, knockdown of RNF4 led to a remarkable increase in PML SUMOylation and the function of PML-NBs, further promoting ATO- or Ang II-induced HERG protein downregulation. Mechanistically, an increase in PML SUMOylation by ATO or Ang II dramatically enhanced the formation of PML and Pin1 complexes in PML-NBs, leading to the upregulation of TGF-ß1 protein, eventually inhibiting HERG expression through activation of protein kinase A. The present work uncovered a novel molecular mechanism underlying HERG protein expression and indicated that PML SUMOylation is a critical step in the development of drug-acquired arrhythmia.