Interpretable Dynamic Directed Graph Convolutional Network for Multi-Relational Prediction of Missense Mutation and Drug Response.

Tumor heterogeneity presents a significant challenge in predicting drug responses, especially as missense mutations within the same gene can lead to varied outcomes such as drug resistance, enhanced sensitivity, or therapeutic ineffectiveness. These complex relationships highlight the need for advanced analytical approaches in oncology. Due to their powerful ability to handle heterogeneous data, graph convolutional networks (GCNs) represent a promising approach for predicting drug responses.

Comprehensive Assessment of BERT-Based Methods for Predicting Antimicrobial Peptides.

In recent years, the prediction of antimicrobial peptides (AMPs) has gained prominence due to their high antibacterial activity and reduced susceptibility to drug resistance, making them potential antibiotic substitutes. To advance the field of AMP recognition, an increasing number of natural language processing methods are being applied. These methods exhibit diversity in terms of pretraining models, pretraining data sets, word vector embeddings, feature encoding methods, and downstream classification models.

TeaTFactor: a prediction tool for tea plant transcription factors based on BERT.

A transcription factor (TF) is a sequence-specific DNA-binding protein, which plays key roles in cell-fate decision by regulating gene expression. Predicting TFs is key for tea plant research community, as they regulate gene expression, influencing plant growth, development, and stress responses. It is a challenging task through wet lab experimental validation, due to their rarity, as well as the high cost and time requirements.

Ultrasound-guided transmuscular quadratus lumborum block reduced postoperative opioids consumptions in patients after laparoscopic hepatectomy: a three-arm randomized controlled trial.

Background: To investigate whether transmuscular quadratus lumborum block (TQLB) combined with oxycodone-based patient-controlled intravenous analgesia (PCIA) compared with sufentanil-based patient-controlled intravenous analgesia could reduce postoperative pain and opioid consumption in patients undergoing laparoscopic hepatectomy.

Methods: Eighty patients undergoing laparoscopic hepatectomy surgery were randomly divided into Group S (Sufentanil for PCIA group), Group O (Oxycodone for PCIA group) and Group QO (transmuscular quadratus lumborum block + oxycodone for PCIA group). Primary outcome was Numerical Rating Scale (NRS) pain score when coughing at 6th hour after the operation.

Induction of heme oxygenase-1 by hemin protects lung against orthotopic autologous liver transplantation-induced acute lung injury in rats.

Background: Post-liver transplantation acute lung injury (ALI) severely affects patients' survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion-induced increased oxidative stress plays a critical role in mediating post-liver transplantation ALI and that induction of heme oxgenase-1 (HO-1), an enzyme with anti-oxidative stress properties, can confer effective protection of lung against ALI.

Methods: Male Sprague-Dawley rats underwent autologous orthotopic liver transplantation (OALT) in the absence or presence of treatments with the selective HO-1 inducer (Hemin) or HO-1 inhibitor (ZnPP).

Intestinal injury following liver transplantation was mediated by TLR4/NF-κB activation-induced cell apoptosis.

Intestinal motility and barriers are often impaired due to intestinal congestion during liver transplantation. Intestinal bacteria and enterogenous endotoxins enter into the blood stream or lymphatic system and translocate to other organs, which can result in postoperative multi-organ dysfunction (MODF) and systemic inflammatory reaction syndrome (SIRS) severely affecting patient survival. However, the mechanisms underlying liver transplantation-induced intestinal injury remain unclear and effective therapies are lacking.

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4-nuclear factor kappa B signaling.

Background: To investigate whether pretreatment with dexmedetomidine (Dex) has a protective effect against acute lung injury (ALI) in an orthotopic autologous liver transplantation (OALT) rat model and to explore the mechanisms responsible for the protective effect of Dex against lung injury.

Methods: Forty-eight rats underwent OALT and were randomly divided into six groups (n = 8 in each group) that received 10 µg/kg Dex, 50 µg/kg Dex, 50 µg/kg Dex + nonspecific α2-adrenergic receptor (AR) antagonist atipamezole, 50 µg/kg Dex + specific α2B/C-AR antagonist ARC-239, 50 µg/kg Dex + specific α2A-AR antagonist BRL-44408, or the same amount of normal saline. The sham rats (n = 8) underwent anesthesia induction, laparotomy, and separation of the portal vein without liver ischemia and reperfusion.

The interaction between oxidative stress and mast cell activation plays a role in acute lung injuries induced by intestinal ischemia-reperfusion.

Background: Both oxidative stress and mast cells are involved in acute lung injuries (ALIs) that are induced by intestinal ischemia-reperfusion (IIR). The aim of this study was to further investigate the interaction between oxidative stress and mast cells during the process of IIR-induced ALI.

Materials And Methods: Thirty adult Sprague-Dawley rats were randomly divided into five groups: sham, IIR, IIR + compound 48/80 (CP), N-acetylcysteine (NAC) + IIR, and NAC + IIR + CP.

Dexamethasone pretreatment alleviates intestinal ischemia-reperfusion injury.

Background: Activated mast cells are involved in the pathogenesis of intestinal ischemia-reperfusion (I/R)-related injury. Dexamethasone has been widely used to protect organs from I/R injury. This study was conducted to investigate the impact of treatment with dexamethasone at different stages of the II/R process on mast cell infiltration and activity and intestinal injury.

Treatment of mice with cromolyn sodium after reperfusion, but not prior to ischemia, attenuates small intestinal ischemia-reperfusion injury.

Stabilizing mast cells (MCs) can either inhibit or augment inflammation; however, how improved therapeutic benefits against small intestinal ischemia-reperfusion injury (IIRI) can be achieved by stabilizing MCs remains to be elucidated. The present study was designed to evaluate different treatments with cromolyn sodium (CS, an MC stabilizer), which was administrated either prior to ischemia or after reperfusion. Kunming mice were randomized into a sham-operated group (SH), a sole IIR group (M), in which mice were subjected to 30 min superior mesenteric artery occlusion followed by 3 day or 3 h reperfusion, or IIR, treated with CS 15 min prior to ischemia or 15 min after reperfusion in the PreCr and PostCr groups.

Time-course analysis of counts and degranulation of mast cells during early intestinal ischemia-reperfusion injury in mice.

Findings of previous studies have revealed that intestinal mucosal mast cells (IMMCs) are involved in small intestinal ischemia‑reperfusion injury (IIRI). However, time-course changes of mast cell counts and mast cell function in this process remain unclear. The present study aimed to observe the number of IMMCs and to investigate the correlation between their activation and small intestine injury at various time points during the period of small intestinal ischemia reperfusion (IIR).

Mast cells activation contribute to small intestinal ischemia reperfusion induced acute lung injury in rats.

Background: Small intestinal ischemia-reperfusion (IIR) injury may lead to severe local and remote tissue injury, especially acute lung injury (ALI). Mast cell activation plays an important role in IIR injury. It is unknown whether IIR mediates lung injury via mast cell activation.

Mast-cell-releasing tryptase triggers acute lung injury induced by small intestinal ischemia-reperfusion by activating PAR-2 in rats.

Mast cell has been demonstrated to be involved in the small intestinal ischemia-reperfusion (IIR) injury, however, the precise role of tryptase released from mast cell on acute lung injury(ALI) induced by IIR remains to be elucidated, our study aimed to observe the roles of tryptase on ALI triggered by IIR and its underlying mechanism. Adult SD rats were randomized into sham-operated group, sole IIR group in which rats were subjected to 75 min superior mesenteric artery occlusion followed by 4 h reperfusion, or IIR being respectively treated with cromolyn sodium, protamine, and compound 48/80. The above agents were, respectively, administrated intravenously 5 min before reperfusion.

Influence of Ketotifen, Cromolyn Sodium, and Compound 48/80 on the survival rates after intestinal ischemia reperfusion injury in rats.

Background: Mast cells were associated with intestinal ischemia-reperfusion injury, the study was to observe the influence of Ketotifen, Cromolyn Sdium(CS), and Compound 48/80(CP) on the survival rates on the third day after intestinal ischemia-reperfusion injury in rats.

Methods: 120 healthy Sprague-Dawley rats were randomly divided into 5 groups, Sham-operated group (group S), model group (group M), group K, group C and group CP. Intestinal damage was triggered by clamping the superior mesenteric artery for 75 minutes, group K, C, and CP were treated with kotifen 1 mg.