Objective: This study investigated the effect of applying different torque values on the sagittal displacement tendency of mandibular incisors during intrusion using clear aligners, with the aim of providing a reference for achieving true vertical intrusion (intrusion without labiolingual movement) of mandibular incisors in clear aligner therapy. Methods: This study was approved by the institutional ethics committee. A volunteer with an incisor mandibular plane angle of 94° was selected. Using cone-beam computed tomography and intraoral scan data, a high-precision three-dimensional finite element model was established. An intrusion amount of 0.2 mm was set for the mandibular incisors, and four simulation groups were defined by applying 0°, 1°, 2°, and 3° of root labial torque. The displacement tendency of the incisors and the stress distribution within the periodontal ligament were analyzed. Results: When 0° of root labial torque was applied, the mandibular incisors exhibited intrusion accompanied by crown-labial, root-lingual inclination. When 1°-3° of root labial torque was applied, the mandibular incisors exhibited intrusion accompanied by the inclination gradually shifted from crown-labial, root-lingual towards crown-lingual, root-labial. Based on the line graph of sagittal displacement, the central incisors and lateral incisors approximated true vertical intrusion when 1.8° and 2.5° of root labial torque was applied, respectively. The mandibular canines consistently exhibited extrusion accompanied by labial crown inclination. Stress within the periodontal ligament of the incisors and canines was primarily concentrated at the root apex and cervical region. After applying root labial torque, the area of stress concentration in the incisors cervical periodontal ligament shifted from the labial side to the lingual side. The stress in the periodontal ligament at the cervical region of the canines is predominantly concentrated on the labial side. Conclusion Applying appropriate torque control during mandibular incisor intrusion with clear aligners facilitates true vertical intrusion, thereby enhancing the efficiency of the intrusion.

BACKGROUND: Chronic kidney disease (CKD) is associated with common pathophysiological processes, such as inflammation and fibrosis, in both the heart and the kidney. However, the underlying molecular mechanisms that drive these processes are not yet fully understood. Therefore, this study focused on the molecular mechanism of heart and kidney injury in CKD. METHODS: We generated an microRNA (miR)-26a knockout (KO) mouse model to investigate the role of miR-26a in angiotensin (Ang)-II-induced cardiac and renal injury. We performed Ang-II modeling in wild type (WT) mice and miR-26a KO mice, with six mice in each group. In addition, Ang-II-treated AC16 cells and HK2 cells were used as in vitro models of cardiac and renal injury in the context of CKD. Histological staining, immunohistochemistry, quantitative real-time polymerase chain reaction (PCR), and Western blotting were applied to study the regulation of miR-26a on Ang-II-induced cardiac and renal injury. Immunofluorescence reporter assays were used to detect downstream genes of miR-26a, and immunoprecipitation was employed to identify the interacting protein of LIM and senescent cell antigen-like domain 1 (LIMS1). We also used an adeno-associated virus (AAV) to supplement LIMS1 and explored the specific regulatory mechanism of miR-26a on Ang-II-induced cardiac and renal injury. Dunnett's multiple comparison and t -test were used to analyze the data. RESULTS: Compared with the control mice, miR-26a expression was significantly downregulated in both the kidney and the heart after Ang-II infusion. Our study identified LIMS1 as a novel target gene of miR-26a in both heart and kidney tissues. Downregulation of miR-26a activated the LIMS1/integrin-linked kinase (ILK) signaling pathway in the heart and kidney, which represents a common molecular mechanism underlying inflammation and fibrosis in heart and kidney tissues during CKD. Furthermore, knockout of miR-26a worsened inflammation and fibrosis in the heart and kidney by inhibiting the LIMS1/ILK signaling pathway; on the contrary, supplementation with exogenous miR-26a reversed all these changes. CONCLUSIONS Our findings suggest that miR-26a could be a promising therapeutic target for the treatment of cardiorenal injury in CKD. This is attributed to its ability to regulate the LIMS1/ILK signaling pathway, which represents a common molecular mechanism in both heart and kidney tissues.
Animals ; MicroRNAs/metabolism* ; Angiotensin II/toxicity* ; Mice ; Renal Insufficiency, Chronic/chemically induced* ; Mice, Knockout ; Disease Models, Animal ; Male ; Signal Transduction/genetics* ; LIM Domain Proteins/genetics* ; Mice, Inbred C57BL ; Cell Line ; Humans

Objective:To observe the effect of old RBCs transfusion on cognitive function in rats and the improvement effect of mi -nocycline.Methods: Male SD rats at the age of 6 months were randomly divided into 4 groups.The RBCs were obtained from male rats by centrifuging the total blood and stored at 4℃.The rats of fresh RBCs group (group F) were transfused with the RBCs stored for 1 day.The rats of old RBCs group (group O) were transfused with the RBCs stored for 7 days.The rats of treatment group (group T) received 40 mg· kg-1 minocycline with intraperitoneal injection before the transfusion .The rats of the control group ( group C) were transfused with the normal saline .The brain levels of IL-1βand IL-6 were determined with Quantikine ELISA kits in 24 hours after the blood transfusion (n=6).The rats were subjected to Barnes maze tests after 1 week of the blood transfusion (n=10).Results:The brain levels of IL-1βand IL-6 in group O were higher than those in group C and F (P<0.05), which were lower in group T than those in group O(P<0.05).The rats of group O spent longer time finding the target box than those of group C and F in the Barnes maze (P<0.05), and the time was shorter in group T than that in group O (P<0.05).Conclusion: Old RBCs transfusion plays a role in neuro-inflammation and induces cognitive dysfunction in rats , which may be improved by minocycline .

The E (envelope) protein is the smallest structural protein in all coronaviruses and is the only viral structural protein in which no variation has been detected. We conducted genome sequencing and phylogenetic analyses of SARS-CoV. Based on genome sequencing, we predicted the E protein is a transmembrane (TM) protein characterized by a TM region with strong hydrophobicity and alpha-helix conformation. We identified a segment (NH2-_L-Cys-A-Y-Cys-Cys-N_-COOH) in the carboxyl-terminal region of the E protein that appears to form three disulfide bonds with another segment of corresponding cysteines in the carboxyl-terminus of the S (spike) protein. These bonds point to a possible structural association between the E and S proteins. Our phylogenetic analyses of the E protein sequences in all published coronaviruses place SARS-CoV in an independent group in Coronaviridae and suggest a non-human animal origin.
Amino Acid Sequence ; Base Sequence ; Cluster Analysis ; Codon ; genetics ; Gene Components ; Genome, Viral ; Membrane Glycoproteins ; metabolism ; Membrane Proteins ; genetics ; metabolism ; Molecular Sequence Data ; Phylogeny ; Protein Conformation ; SARS Virus ; genetics ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Homology ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins ; genetics ; metabolism