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ABSTRACT Objectives Materials and Methods Results Conclusions To evaluate and compare the accuracy of task‐autonomous robot‐assisted implant surgery (RAIS) and dynamic computer‐assisted implant surgery (dCAIS) for zygomatic implant placement.Ten atrophic edentulous maxilla models requiring zygomatic implant (ZI) placement were randomly divided into the RAIS and dCAIS groups. Osteotomies and implant placement were performed under the guidance of a task‐autonomous robotic system or dynamic navigation system. A total of 20 ZIs were analyzed. The angular, coronal, lateral coronal, coronal depth, apical, lateral apical, and apical depth deviations were measured and analyzed between the two groups. The primary outcome parameters were the angular deviations between the planned and the placed ZIs. Data was subjected to descriptive and comparative statistical analysis. The significance of inter‐group differences for continuous variables was assessed with Student's two‐sample t‐tests, Welch two‐sample t‐tests, and Mann–Whitney U tests according to the distribution normality and variance homogeneity.ZI placement deviations were compared between the RAIS and dCAIS groups, showing a mean angular deviation of 0.92 ± 0.40° versus 2.03 ± 0.53° (p < 0.001), a mean (±SD) coronal deviation of 0.48 ± 0.25 mm versus 1.29 ± 0.46 mm (p < 0.001), and a mean apical deviation of 0.88 ± 0.28 mm versus 1.96 ± 0.46 mm (p < 0.001).For computer‐guided ZI placement, task‐autonomous RAIS was superior to dCAIS in terms of accuracy. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Purpose Methods and Materials Results Conclusions The learning curve effect of dynamic computer‐assisted implant surgery (D‐CAIS) was observed among inexperienced novice surgeons. The learning curves can provide valuable information for novice surgeons and valid comparisons between new and conventional techniques. Recently, robotic computer‐assisted implant surgery (R‐CAIS) has shown promise as a novel dental implant surgical technique for both partially and edentulous patients. However, its learning curve remains unknown.The aim of this study was to explore the learning curve of dental implant placement surgery with a task‐autonomous robotic system among young dentists with different specialties.Four young dentists (mean age: 25.3 ± 1.5 years at the beginning of their first attempt) with equal representation of males and females and with different specialties participated in this study. None of the participants had prior experience in R‐CAIS. Each operator placed eight implants over eight attempts using a semi‐active task‐autonomous robotic system. Among the eight implants, four were straight lateral incisor implants, and four were 30°‐tilted premolar implants. The implants were placed in each dental quadrant of the maxillary and mandibular jaw modules. The operation time was recorded. Coronal, apical, and angular deviations between the planned and actual sites of implant placement were measured by merging preoperative and postoperative cone‐beam computed tomography (CBCT) scans. The data were analyzed with repeated‐measures ANOVA (α = 0.05).The mean time for implant placement was associated with the number of attempts (p < 0.01). The time taken for the second attempt was significantly shorter than that of the first attempt (33.26 vs. 30.47 min; p < 0.001) then it plateaued. Three‐dimensional (3D) angular (p = 0.31), coronal deviation (p = 0.26), and apical deviation (p = 0.06) did not differ significantly among attempts. The mean values and standard deviations of 3D coronal deviation, 3D apical deviation, and 3D angular deviation were 0.71 ± 0.31 mm, 0.72 ± 0.30 mm, and 0.94 ± 0.58°, respectively. Neither the position of the jaw (p > 0.59) nor the tilt angle of the implant (straight or 30°‐tilted, p > 0.85) was related to implant placement accuracy.Dentists quickly learned the basic workflow of R‐CAIS and thus facilitated the clinicians in the mastery of implant placement on edentulous jaw modules, leading to a comparable operating speed and high precision. Moreover, the accuracy of placement of straight and tilted implants in both the maxilla and mandible with R‐CAIS was satisfactory. [ABSTRACT FROM AUTHOR]

Background: With ubiquitous social media platforms, people express their thoughts and emotions, making social media data valuable for studying and detecting depression symptoms. Objective: First, we detect depression by leveraging textual, visual, and auxiliary features from the Weibo social media platform. Second, we aim to comprehend the reasons behind the model's results, particularly in medicine, where trust is crucial. Methods: To address challenges such as varying text lengths and abundant social media data, we employ a text extension technique to standardize text length, enhancing model robustness and semantic feature learning accuracy. We utilize tree‐long short‐term memory and bidirectional gate recurrent unit models to capture long‐term and short‐term dependencies in text data, respectively. To extract emotional features from images, the integration of optical character recognition (OCR) technology with an emotion lexicon is employed, addressing the limitations of OCR technology in accuracy when dealing with complex or blurred text. In addition, auxiliary features based on social behaviour are introduced. These modalities' output features are fed into an attention fusion network for effective depression indicators. Results: Extensive experiments validate our methodology, showing a precision of 0.987 and recall rate of 0.97 in depression detection tasks. Conclusions: By leveraging text, images, and auxiliary features from Weibo, we develop text picture sentiment auxiliary (TPSA), a novel depression detection model. we ascertained that the emotional features extracted from images and text play a pivotal role in depression detection, providing valuable insights for the detection and assessment of the psychological disorder. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to compare the accuracy of dental implant placement in a single tooth gap, including the postextraction site and healed site, using a task‐autonomous robotic system and a dynamic navigation system. Materials and Methods: Forty partially edentulous models requiring both immediate and conventional implant placement were randomly divided into a robotic system group and a navigation system group. The coronal, apical, and angular deviations of the implants were measured and assessed between the groups. Results: The deviations in immediate implant placement were compared between the robotic system and dynamic navigation system groups, showing a mean (±SD) coronal deviation of 0.86 ± 0.36 versus 0.70 ± 0.21 mm (p =.101), a mean apical deviation of 0.77 ± 0.34 versus 0.95 ± 0.38 mm (p =.127), and a mean angular deviation of 1.94 ± 0.66° versus 3.44 ± 1.38° (p <.001). At the healed site, significantly smaller coronal deviation (0.46 ± 0.29 vs. 0.70 ± 0.30 mm, p =.005), apical deviation (0.56 ± 0.30 vs. 0.85 ± 0.25 mm, p <.001), and angular deviation (1.36 ± 0.54 vs. 1.80 ± 0.70 mm, p =.034) were found in the robotic system group than in the dynamic navigation group. Conclusions: The position in both immediate and conventional implant placement was more precise with the task‐autonomous robotic system than with the dynamic navigation system. Its performance in actual clinical applications should be confirmed in further trials. [ABSTRACT FROM AUTHOR]

Lysosomal dysfunction can drive carcinogenesis. Lysosomal‐associated membrane protein 3 (LAMP3), is a member of the Lysosome Associated Membrane Proteins and is involved in the malignant phenotype such as tumour metastasis and drug resistance, while the mechanisms that regulate the malignant progression of tumour remain vague. Our study aims to provide a more systematic and comprehensive understanding of the role of LAMP3 in the progression of various cancers by various databases.We explored the role of LAMP3 in pan‐cancer using The Cancer Genome Atlas (TCGA) and Genotype‐Tissue Expression (GTEx) database. Multiple online web platforms and software were used for data analysis, including HPA, TIMER, TISIDB, GEPIA, UALCAN, Kaplan–Meier plotter, DAVID and TIGER. The immunohistochemistry was used to quantify the LAMP3 and PD‐L1 expression levels in cancer.High LAMP3 expression was found in most cancers and differentially expressed across molecular and immune subtypes. The expression of LAMP3 was involved in the immune‐associated processes of Antigen processing and presentation, Th17 cell differentiation, Th1 and Th2 cell differentiation, and the immune‐associated pathways of T cell receptor and B cell receptor signalling pathways in most cancers. It also correlated with genetic markers of immunomodulators in various cancers. LAMP3 and PD‐L1 expression in BRCA and HNSC tissues was higher than that in corresponding adjacent normal tissues by immunohistochemistry. There is a significant correlation between the expression of LAMP3 and PD‐L1.Our study elucidates that LAMP3 has different expression patterns and genetic alteration patterns in different tumours. It is a potential biomarker for immune‐related cancer diagnosis, prognosis and efficacy prediction. [ABSTRACT FROM AUTHOR]

Ulcerative colitis (UC) pathogenesis is largely associated with intestinal epithelial barrier dysfunction. A therapeutic approach to UC involves the repair of damaged intestinal barrier. Our study aimed to investigate whether aryl hydrocarbon receptor (AhR) mediated the intestinal barrier repair effects of quercetin to ameliorate UC. 3% dextran sulfate sodium was used to induce colitic mice, and quercetin (25, 50, and 100 mg/kg) was administered orally for 10 days to assess the therapeutic effects. In vitro, Caco‐2 cells were used to explore the effect of quercetin on tight junction protein expression and AhR activation. The results showed that quercetin alleviated colitic mice by restoring tight junctions (TJs) integrity via an AhR‐dependent manner (p < 0.05). In vitro, quercetin dose‐dependently elevated the expressions of TJs protein ZO‐1 and Claudin1, and activated AhR by enhancing the expression of CYP1A1 and facilitating AhR nuclear translocation in Caco‐2 cells (p < 0.05). While AhR antagonist CH223191 reversed the therapeutic effects of quercetin (p < 0.05) and blocked quercetin‐induced AhR activation and enhancement of TJs protein (p < 0.05). In conclusion, quercetin repaired intestinal barrier dysfunction by activating AhR‐mediated enhancement of TJs to alleviate UC. Our research offered new perspectives on how quercetin enhanced intestinal barrier function. [ABSTRACT FROM AUTHOR]

The treatment of combination drugs in complex diseases has been spotlighted. Ulcerative colitis (UC) is a chronic inflammatory disease that has made progress in combination therapy. Baicalin, a flavone from Scutellaria baicalensis Georgi. (Lamiaceae), and emodin, an anthraquinone derivative from Rhei Radix et Rhizoma. (Polygonaceae), both have been reported to possess antiinflammatory activities. Our study investigated whether combined treatment with baicalin and emodin had a synergistic effect in inhibiting colitis inflammation. The results showed that baicalin combined with emodin at a lower dose had the same effect as the two drugs alone significantly alleviated the symptoms of dextran sulfate sodium (DSS)-induced colitis mice, involving the prevention of the loss of body weight and colon shortening, the decrease in the disease activity index (DAI), and intestinal damages. The combined treatment decreased the expression of CD14/TLR4/NF-κB pathway proteins and increased the expression of PPAR-γ protein in the colon of colitis mice. Further study in vitro has shown that baicalin decreased the expression of CD14, whereas emodin increased the expression of PPAR-γ, both of which inhibited the activity of NF-κB and exerted antiinflammatory effects. Furthermore, compared to the treatment using the two drugs individually, baicalin combined with emodin had more significant effects on the expression of CD14 and PPAR-γ. Therefore, emodin combined with baicalin had a synergistic effect on DSS-induced colitis. [ABSTRACT FROM AUTHOR]

Background The renin-angiotensin system plays a crucial role in the development of heart failure, and Ang II (angiotensin II) acts as the critical effector of the renin-angiotensin system in regulating cardiac fibrosis. However, the mechanisms of cardiac fibrosis are complex and still not fully understood. IGF1R (insulin-like growth factor 1 receptor) has multiple functions in maintaining cardiovascular homeostasis, and low-dose IGF1 treatment is effective in relieving Ang II-induced cardiac fibrosis. Here, we aimed to investigate the molecular mechanism of IGF1R in Ang II-induced cardiac fibrosis. Methods and Results Using primary mouse cardiac microvascular endothelial cells and fibroblasts, in vitro experiments were performed. Using C57BL/6J mice and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9)-mediated IGF1R heterozygous knockout ( Igf1r +/- ) mice, cardiac fibrosis mouse models were induced by Ang II for 2 weeks. The expression of IGF1R was examined by quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot. Mice heart histologic changes were evaluated using Masson and picro sirius red staining. Fibrotic markers and signal molecules indicating the function of the Akt (protein kinase B)/ERK (extracellular signal-regulated kinase)/nuclear factor-κB pathway were detected using quantitative reverse transcription polymerase chain reaction and Western blot. RNA sequencing was used to explore IGF1R-mediated target genes in the hearts of mice, and the association of IGF1R and G-protein-coupled receptor kinase 5 was identified by coimmunoprecipitation. More important, blocking IGF1R signaling significantly suppressed endothelial-mesenchymal transition in primary mouse cardiac microvascular endothelial cells and mice in response to transforming growth factor-β1 or Ang II, respectively. Deficiency or inhibition of IGF1R signaling remarkably attenuated Ang II-induced cardiac fibrosis in primary mouse cardiac fibroblasts and mice. We further observed that the patients with heart failure exhibited higher blood levels of IGF1 and IGF1R than healthy individuals. Moreover, Ang II treatment significantly increased cardiac IGF1R in wild type mice but led to a slight downregulation in Igf1r +/- mice. Interestingly, IGF1R deficiency significantly alleviated cardiac fibrosis in Ang II-treated mice. Mechanistically, the phosphorylation level of Akt and ERK was upregulated in Ang II-treated mice, whereas blocking IGF1R signaling in mice inhibited these changes of Akt and ERK phosphorylation. Concurrently, phosphorylated p65 of nuclear factor-κB exhibited similar alterations in the corresponding group of mice. Intriguingly, IGF1R directly interacted with G-protein-coupled receptor kinase 5, and this association decreased ≈50% in Igf1r +/- mice. In addition, Grk5 deletion downregulated expression of the Akt/ERK/nuclear factor-κB signaling pathway in primary mouse cardiac fibroblasts. Conclusions IGF1R signaling deficiency alleviates Ang II-induced cardiac fibrosis, at least partially through inhibiting endothelial-mesenchymal transition via the Akt/ERK/nuclear factor-κB pathway. Interestingly, G-protein-coupled receptor kinase 5 associates with IGF1R signaling directly, and it concurrently acts as an IGF1R downstream effector. This study suggests the promising potential of IGF1R as a therapeutic target for cardiac fibrosis.