Explore the vast range of titles available.

Background Frailty is a dynamic process, but its changes following surgery are unclear. This study aimed to investigate frailty change trajectories and their risk factors in older patients undergoing gastrointestinal tumor surgery. Methods The Frail Scale (FS) assessed frailty from preoperative to 180 days after surgery. The latent class analysis (LCA) was established to identify the most fitting latent class, and the risk factors of these change trajectories were analyzed. We also recorded and explored changes in FS components. Results 212 elderly patients (aged ≥ 60 years) scheduled for gastrointestinal tumor surgery under general anesthesia completed the study. The LCA identified four optimal trajectory groups. There are differences in gender, age, marriage, American Society of Anesthesiologists (ASA) classification, number of comorbidities, hemoglobin, Charlson comorbidity index (CCI), the six-minute walk test (6MWT), metabolic equivalent (MET), preoperative frailty status, and time to first ambulation among the four groups ( P  < 0.05). Comorbidities, MET, preoperative frailty, age, first time to ambulation, and 6WMT were independent factors influencing abnormal frailty trajectories. Overall, the FS components all changed 180 days after the surgery. Except for weight loss, the changes in the other components were related to the surgical site ( P  < 0.05). Conclusion Frailty is a dynamic process. Older patients with more comorbidities, low MET and 6WMT, preoperative frailty, and later time to ambulation are prone to remain in frailty or transition to it after surgery. Clinical attention and targeted rehabilitation should be provided to them.

It has been recognized that iron overload may harm the body’s health. Vascular endothelial cells (VECs) are one of the main targets of iron overload injury, and the mechanism involved was thought to be related to the excessive generation of reactive oxygen species (ROS). However, the subcellular and temporal characteristics of ROS generation, potential downstream mechanisms, and target organelles in VECs injured by iron overload have not been expounded yet. In this study, we elucidated the abovementioned issues through both in vivo and in vitro experiments. Mice were fed pellet diets that were supplemented with iron for 4 consecutive months. Results showed that the thoracic aortic strips’ endothelium-dependent dilation was significantly impaired and associated with inflammatory changes, noticeable under brown TUNEL-positive staining in microscopy analysis. In addition, the serum content of asymmetric dimethylarginine (ADMA) increased, whereas nitric oxide (NO) levels decreased. Furthermore, the dimethylarginine dimethylaminohydrolase II (DDAHII) expression and activity, as well as the phosphorylation of endothelial nitric oxide synthase (eNOS) in aortic tissue, were inhibited. Human umbilical vein endothelial cells were treated with 50 μM iron dextran for 48 hours, after which the cell viability, NO content, DDAHII expression and activity, and phosphorylation of eNOS decreased and lactate dehydrogenase and caspase-3 activity, ADMA content, and apoptotic cells significantly increased. After the addition of L-arginine (L-Arg) or pAD/DDAHII, the abovementioned changes were reversed. By dynamically detecting the changes of ROS generation in the cytoplasm and mitochondria and interfering with different aspects of signaling pathways, we have confirmed for the first time that excessive ROS originates from the cytoplasm and activates the ROS-induced ROS release (RIRR) mechanism, leading to mitochondrial dysfunction. Together, our data suggested that excessive free iron ions produced excess ROS in the cytoplasm. Thus, excess ROS create one vicious circle by activating the ADMA/eNOS/DDAHII/NO pathway and another vicious circle by activation of the RIRR mechanism, which, when combined, induce a ROS burst, resulting in mitochondrial dysfunction and damaged VECs.

Iron overload is harmful to health and associates with intracellular excessive reactive oxygen species (ROS) generation. Nobiletin (Nob) is known to be antioxidant and anti-inflammatory. However, whether Nob can protect endothelial cells against iron overload has not been studied, and the specific mechanism has not yet been elucidated. In this study, we have identified the protective effects of Nob, and its underlying molecular mechanism in human umbilical vein endothelial cells (HUVECs) suffered from iron overload via ROS/ADMA/DDAHII/eNOS/NO pathway. We found that compared with 50 μM iron dextran treatment, co-treatment with 20 μM Nob increased cell viability and decreased lactate dehydrogenase activity. Besides, Nob could upregulate DDAHII expression and activity, promote eNOS phosphorylation to produce more NO, reduce ADMA content, and therefore increase superoxide dismutase, catalase, and glutathione peroxidase activities, and decrease malondialdehyde level and ROS generation. Nob also inhibited mitochondrial permeability transition pore (mPTP) openness and cleaved caspase-3 expression, and decreased apoptosis induced by iron overload. These results were consistent when Nob was replaced by the positive control reagents L-arginine (a competitive substrate of ADMA), cyclosporin A (an mPTP closing agent), or edaravone (a free radical scavenger). The addition of pAD/DDAHII-shRNA adenovirus reversed the above effects of Nob. These data suggested that the protective mechanism of Nob was to inhibit ROS burst, upregulate DDAHII expression and activity, promote eNOS phosphorylation, produce NO, reduce ADMA content, and ultimately alleviate iron overload damage in vascular endothelium.

Ternesite is an intermediate phase formed during clinkering of calcium sulfoaluminate (CSA) cement. This paper presents an experimental study on the feasibility of using ternesite as an additive of CSA cement in order to improve cement properties. Properties including setting time, mechanical strength, dimensional stability and hydration kinetics are investigated. The results indicated that the incorporation of ternesite can decrease the setting times and the strength development at early ages. The hydration of ternesite at later ages can increase the strength after 28 days of hydration, and 5% of ternesite is most favorable. The use of ternesite as an additive in CSA cement is harmless to the volume stability. The addition of ye’elimite to the pure ternesite promotes the hydration of ternesite and the formation of ettringite. XRD results show that the addition of ternesite can promote the formation of ettringite at later ages.

Sulfate-rich belite sulfoaluminate (BSA) cements with varied phase compositions were synthesized in this work. The presence of sulfate in the clinker is in the form of anhydrite in addition to calcium sulfoaluminate. The aim of this paper is to study the effect of mineral composition on cement properties. Experimental results indicate that the improvement of early-age strengths mainly depends on the hydration of ye’elimite. The increase of ferrite content promotes the compressive strength after 7 days of hardening, but has adverse effect on cement strength at early ages. The optimum content of ferrite is between 10 and 20% for BSA cement containing approximately 35% ye’elimite. Different amounts of natural gypsum were added to the synthetic sulfate-rich BSA clinkers and we found that anhydrite formed in BSA clinkers can replace natural gypsum to facilitate the hydration of ye’elimite.

Small nuclear RNAs (snRNAs) play essential roles in spliceosome assembly and splicing. Most snRNAs are transcribed by the DNA-dependent RNA polymerase II (Pol II) and require 39-end endonucleolytic cleavage. We have previously shown that the Arabidopsis (Arabidopsis thaliana) Defective in snRNA Processing 1 (DSP1) complex, composed of at least five subunits, is responsible for snRNA 3' maturation and is essential for plant development. Yet it remains unclear how DSP1 complex subunits act together to process snRNAs. Here, we show that DSP4, a member of the metallo-𝛽-lactamase family, physically interacts with DSP1 through its 𝛽-Casp domain. Null dsp4-1 mutants have pleiotropic developmental defects, including impaired pollen development and reduced pre-snRNA transcription and 3' maturation, resembling the phenotype of the dsp1-1 mutant. Interestingly, dsp1-1 dsp4-1 double mutants exhibit complete male sterility and reduced pre-snRNA transcription and 3'-end maturation, unlike dsp1-1 or dsp4-1. In addition, Pol II occupancy at snRNA loci is lower in dsp1-1 dsp4-1 than in either single mutant. We also detected miscleaved pre-snRNAs in dsp1-1 dsp4-1, but not in dsp1-1 or dsp4-1. Taken together, these data reveal that DSP1 and DSP4 function is essential for pollen development, and that the two cooperatively promote pre-snRNA transcription and 3'-end processing efficiency and accuracy.

Small nuclear RNAs (snRNAs) play essential roles in spliceosome assembly and splicing. Most snRNAs are transcribed by the DNA-dependent RNA polymerase II (Pol II) and require 3'-end endonucleolytic cleavage. We have previously shown that the Arabidopsis (Arabidopsis thaliana) Defective in snRNA Processing 1 (DSP1) complex, composed of at least five subunits, is responsible for snRNA 3' maturation and is essential for plant development. Yet it remains unclear how DSP1 complex subunits act together to process snRNAs. Here, we show that DSP4, a member of the metallo-β-lactamase family, physically interacts with DSP1 through its β-Casp domain. Null dsp4-1 mutants have pleiotropic developmental defects, including impaired pollen development and reduced pre-snRNA transcription and 3' maturation, resembling the phenotype of the dsp1-1 mutant. Interestingly, dsp1-1 dsp4-1 double mutants exhibit complete male sterility and reduced pre-snRNA transcription and 3'-end maturation, unlike dsp1-1 or dsp4-1. In addition, Pol II occupancy at snRNA loci is lower in dsp1-1 dsp4-1 than in either single mutant. We also detected miscleaved pre-snRNAs in dsp1-1 dsp4-1, but not in dsp1-1 or dsp4-1. Taken together, these data reveal that DSP1 and DSP4 function is essential for pollen development, and that the two cooperatively promote pre-snRNA transcription and 3'-end processing efficiency and accuracy.