Deep learning-based automatic segmentation of bone graft material after maxillary sinus augmentation.

OBJECTIVES: To investigate the accuracy and reliability of deep learning in automatic graft material segmentation after maxillary sinus augmentation (SA) from cone-beam computed tomography (CBCT) images. MATERIALS AND METHODS: One hundred paired CBCT scans (a preoperative scan and a postoperative scan) were collected and randomly allocated to training (n = 82) and testing (n = 18) subsets. The ground truths of graft materials were labeled by three observers together (two experienced surgeons and a computer engineer). A deep learning model including a 3D V-Net and a 3D Attention V-Net was developed. The overall performance of the model was assessed through the testing data set. The comparative accuracy and inference time consumption of the model-driven and manual segmentation (by two surgeons with 3 years of experience in dental implant surgery) were conducted on 10 CBCT scans from the test samples. RESULTS: The deep learning model had a Dice coefficient (Dice) of 90.36 ± 2.53%, a 95% Hausdorff distance (HD) of 1.59 ± 0.82 mm, and an average surface distance (ASD) of 0.38 ± 0.11 mm. The proposed model only needed 7.2 s, while the surgeon took 19.15 min on average to complete a segmentation task. The overall performances of the model were significantly superior to those of surgeons. CONCLUSIONS: The proposed deep learning model yielded a more accurate and efficient performance of automatic segmentation of graft material after SA than that of the two surgeons. The proposed model could facilitate a powerful system for volumetric change evaluation, dental implant planning, and digital dentistry.

Acetylation in pathogenesis: Revealing emerging mechanisms and therapeutic prospects.

Protein acetylation modifications play a central and pivotal role in a myriad of biological processes, spanning cellular metabolism, proliferation, differentiation, apoptosis, and beyond, by effectively reshaping protein structure and function. The metabolic state of cells is intricately connected to epigenetic modifications, which in turn influence chromatin status and gene expression patterns. Notably, pathological alterations in protein acetylation modifications are frequently observed in diseases such as metabolic syndrome, cardiovascular disorders, and cancer. Such abnormalities can result in altered protein properties and loss of function, which are closely associated with developing and progressing related diseases. In recent years, the advancement of precision medicine has highlighted the potential value of protein acetylation in disease diagnosis, treatment, and prevention. This review includes provocative and thought-provoking papers outlining recent breakthroughs in acetylation modifications as they relate to cardiovascular disease, mitochondrial metabolic regulation, liver health, neurological health, obesity, diabetes, and cancer. Additionally, it covers the molecular mechanisms and research challenges in understanding the role of acetylation in disease regulation. By summarizing novel targets and prognostic markers for the treatment of related diseases, we aim to contribute to the field. Furthermore, we discuss current hot topics in acetylation research related to health regulation, including N4-acetylcytidine and liquid-liquid phase separation. The primary objective of this review is to provide insights into the functional diversity and underlying mechanisms by which acetylation regulates proteins in disease contexts.

Adverse Effects of Prenatal Exposure to Oxidized Black Carbon Particles on the Reproductive System of Male Mice.

Ambient black carbon (BC), a main constituent of atmospheric particulate matter (PM), is a primary particle that is mainly generated by the incomplete combustion of fossil fuel and biomass burning. BC has been identified as a potential health risk via exposure. However, the adverse effects of exposure to BC on the male reproductive system remain unclear. In the present study, we explored the effects of maternal exposure to oxidized black carbon (OBC) during pregnancy on testicular development and steroid synthesis in male offspring. Pregnant mice were exposed to OBC (467 µg/kg BW) or nanopure water (as control) by intratracheal instillation from gestation day (GD) 4 to GD 16.5 (every other day). We examined the testicular histology, daily sperm production, serum testosterone, and mRNA expression of hormone synthesis process-related factors of male offspring at postnatal day (PND) 35 and PND 84. Histological examinations exhibited abnormal seminiferous tubules with degenerative changes and low cellular adhesion in testes of OBC-exposed mice at PND 35 and PND 84. Consistent with the decrease in daily sperm production, the serum testosterone level of male offspring of OBC-exposed mice also decreased significantly. Correspondingly, mRNA expression levels of hormone-synthesis-related genes (i.e., StAR, P450scc, P450c17, and 17ß-HSD) were markedly down-regulated in male offspring of PND 35 and PND 84, respectively. In brief, these results suggest that prenatal exposure has detrimental effects on mouse spermatogenesis in adult offspring.

Lethal and Sublethal Toxicity of Beta-Carboline Alkaloids from Peganum harmala (L.) against Aedes albopictus Larvae (Diptera: Culicidae).

Plant-derived agents are powerful bio-pesticides for the eco-friendly control of mosquito vectors and other blood-sucking arthropods. The larval toxicity of beta-carboline alkaloids against the Asian tiger mosquito, Aedes albopictus (Skuse) (Diptera: Culicidae), was investigated under laboratory conditions. The total alkaloid extracts (TAEs) and beta-carboline alkaloids (harmaline, harmine, harmalol, and harman) from Peganum harmala seeds were isolated and tested in this bioassay. All alkaloids were tested either individually or as binary mixtures, using the co-toxicity coefficient (CTC) and Abbott's formula analysis. The results revealed considerable toxicity of the tested alkaloids against A. albopictus larvae. When all larval instars were exposed to the TAEs at 48 h post-treatment, the mortality of all larval instars varied in a concentration-dependent manner. The second-instar larvae were the most susceptible to different concentrations of TAEs, and the fourth-instar larvae were more tolerant to TAEs than the second-instar larvae. Especially, the third-instar larvae exposed to all alkaloids also showed that all doses resulted in an increased mortality of the third-instar larvae at 48 h post-treatment, and the toxicities of the tested alkaloids in a descending order were TAEs > harmaline > harmine > harmalol, with the LC50 values of 44.54 ± 2.56, 55.51 ± 3.01, 93.67 ± 4.53, and 117.87 ± 5.61 µg/mL at 48 h post-treatment, respectively. In addition, all compounds were also tested individually or in a 1:1 ratio (dose LC25/LC25) as binary mixtures to assess the synergistic toxicity of these binary combinations against the third-instar larvae at 24 and 48 h post-treatment, respectively. The results demonstrated that when tested as a binary mixture, all compounds (especially TAEs, harmaline, and harmine) showed their synergistic effects, exceeding the toxicity of each compound alone. Interestingly, the obtained data further revealed that the TAEs at sublethal doses (LC10 and LC25) could significantly delay the larval development and decrease the pupation and emergence rates of A. albopictus. This phenomenon could be helpful in order to develop more effective control strategies for different notorious vector mosquitoes.

AgNPs reduce reproductive capability of female mouse for their toxic effects on mouse early embryo development.

Silver nanoparticles (AgNPs) are widely applied in the field of personal protection for their powerful toxic effects on cells, and recently, a new type of vaginal gel with AgNPs is used to protect the female reproductive tract from microbes and viruses. However, a high risk of AgNPs to the fetus and the underlying mechanism of AgNPs to interfere in embryo development still remain unclear. Thus, this study investigated the impact of two drugs of vaginal gel with AgNPs on reproductive capability of the female mouse by animal experiment. Then, kinetics of AgNPs affecting embryo development was investigated by in vitro embryos culturing, and cell membrane potential (CMP) of zygotes was analyzed by DiBAC4(3) staining. Results indicated that one of the drugs of vaginal gel certainly injured embryo development in spite of no apparent histological change found in ovaries and uteruses of drug-treated mice. In vitro embryo culturing discovered that the toxic effect of AgNPs on embryo development presented particle sizes and dose dependent, and AgNP treatment could rapidly trigger depolarization of the cell membrane of zygotes. Moreover, AgNPs changed the gene expression pattern of Oct-4 and Cdx2 in blastocysts. All these findings suggest that AgNPs can interfere with normal cellular status including cell membrane potential, which has not been noticed in previous studies on the impact of AgNPs on mammalian embryos. Thus, findings of this study alarm us the risk of applying vaginal gel with AgNPs in individual caring and protection of the female reproductive system.

AgNPs reduce reproductive capability of female mouse for their toxic effects on mouse early embryo development.

Silver nanoparticles (AgNPs) are widely applied in the field of personal protection for their powerful toxic effects on cells, and recently, a new type of vaginal gel with AgNPs is used to protect the female reproductive tract from microbes and viruses. However, a high risk of AgNPs to the fetus and the underlying mechanism of AgNPs to interfere in embryo development still remain unclear. Thus, this study investigated the impact of two drugs of vaginal gel with AgNPs on reproductive capability of the female mouse by animal experiment. Then, kinetics of AgNPs affecting embryo development was investigated by in vitro embryos culturing, and cell membrane potential (CMP) of zygotes was analyzed by DiBAC4(3) staining. Results indicated that one of the drugs of vaginal gel certainly injured embryo development in spite of no apparent histological change found in ovaries and uteruses of drug-treated mice. In vitro embryo culturing discovered that the toxic effect of AgNPs on embryo development presented particle sizes and dose dependent, and AgNP treatment could rapidly trigger depolarization of the cell membrane of zygotes. Moreover, AgNPs changed the gene expression pattern of Oct-4 and Cdx2 in blastocysts. All these findings suggest that AgNPs can interfere with normal cellular status including cell membrane potential, which has not been noticed in previous studies on the impact of AgNPs on mammalian embryos. Thus, findings of this study alarm us the risk of applying vaginal gel with AgNPs in individual caring and protection of the female reproductive system.

Low-dose combined exposure of carboxylated black carbon and heavy metal lead induced potentiation of oxidative stress, DNA damage, inflammation, and apoptosis in BEAS-2B cells.

Black carbon (BC) and heavy metal lead (Pb), as typical components of atmospheric PM2.5, have been shown to cause a variety of adverse health effects. However, co-exposure to BC and Pb may induce pulmonary damage by aggravating toxicity via an unknown mechanism. This study aimed to investigate the combined toxicity of carboxylated black carbon (c-BC) and lead acetate (Pb) on human bronchial epithelial cells (BEAS-2B) at the no-observed-adverse-effect level (NOAEL). Cells were exposed to c-BC (6.25 µg/mL) and Pb (4 µg/mL) alone or their combination, and their combined toxicity was investigated by focusing on cell viability, oxidative stress, DNA damage, mitochondrial membrane potential (MMP), apoptosis, and cellular inflammation. Factorial analyses were also used to determine the potential interactions between c-BC and Pb. The results suggested that the combination of c-BC and Pb could significantly increase the production of reactive oxygen species (ROS), malondialdehyde (MDA), and lactate dehydrogenase leakage (LDH) and decrease the activities of glutathione (GSH) and superoxide dismutase (SOD). The excessive oxidative stress could increase the levels of inflammatory cytokine IL-6 and TNF-α, and induce oxidative DNA damage and dissipation of MMP. Moreover, the results also suggested that the combined group could enhance the cellular apoptotic rate and the activation of apoptotic markers like caspase-3, caspase-8, and caspase-9. The factorial analysis further demonstrated that synergistic interaction was responsible for the combined toxicity of c-BC and Pb co-exposure. Most noticeably, the co-exposure of c-BC and Pb could induce some unexpected toxicity, even beyond the known toxicities of the individual compounds in BEAS-2B cells at the NOAEL.

In vitro and in vivo toxic effects and inflammatory responses induced by carboxylated black carbon-lead complex exposure.

Black carbon (BC) is a key component of atmospheric fine particulate matter (PM2.5) and it tends to adsorb various pollutants (e.g., heavy metals and organics) during atmospheric transport. This adsorption leads to the complexity and uncertainty of the source and chemical composition of PM2.5, making the toxicologic effects and health risks induced by PM2.5 difficult to determine. Here, we used carboxylated black carbon (c-BC) and c-BC-lead complexes (c-BC-Pb) to investigate the in vitro and in vivo toxic effects and inflammatory responses. The physicochemical properties of c-BC and c-BC-Pb complexes were characterized by the transmission electron microscope (TEM), X-ray photoelectron spectroscopy (XPS), dynamic light scattering (DLS), and in ductively coupled plasma-atomic emission spectra (ICP-AES). Cytotoxicity in vitro showed that the exposure of human bronchial epithelial cells (BEAS-2B) to low-dose c-BC-Pb particles significantly induced greater toxicity than that of c-BC, suggesting that lead (Pb) might play an important role in induced cytotoxicity after combined exposure to c-BC-Pb particles. The findings were further confirmed by the results in vivo, which indicated that c-BC-Pb particles significantly induced inflammation and lung injury. Based on the results of this experiment, the differences in toxicity can be attributed to the synergistic effect of Pb on the BC particles, which play a synergistic role in vitro and in vivo in the development of toxicity. The c-BC-Pb particles model used in this study may be helpful for the evaluation of cytotoxicity induced by different sources of BC particles or BC-heavy metal complexes and provide a new approach for understanding PM2.5-induced toxicity and health risks.

Insights into the binding behavior of bovine serum albumin to black carbon nanoparticles and induced cytotoxicity.

Black carbon (BC) is a main component of particulate matter (PM2.5). Due to their small size (<100nm), inhaled ultrafine BC nanoparticles may penetrate the lung alveoli, where they interact with surfactant proteins and lipids, causing more serious damage to human health. Here, BC was analyzed to investigate the binding mechanism of its interaction with protein and induction of cytotoxicity changes. The binding process and protein conformation between BC and a serum protein (bovine serum albumin, BSA) were monitored by using a fluorescence quenching technique and UV-vis absorption, Fourier transform infrared (FTIR) and circular dichroism (CD) spectroscopies. The experimental results revealed that the fluorescence quenching of BSA induced by BC was a static quenching process and the hydrophobic force played the critical role in the interaction. The native conformation of BSA on the BC surface was slightly disturbed but obvious structural unfolding of the secondary structure did not occur. In the cytotoxicity study, BC nanoparticles with low concentrations exhibited strong toxicity towards BEAS-2B cells. However, the toxicity of BC nanoparticles could be mitigated by the presence of BSA. Therefore, proteins in biological fluids likely reduce the toxic effect of BC on human health. These findings delineated the binding mechanism and the toxicity between BC and the BSA-BC system, contributing to the understanding of the biological effects of BC exposure on human health in polluted atmospheres.

[Avian diversity and bird strike risk at Fuyang Airport].

From June 2008 to January 2010, a survey of avian communities was conducted in five habitats (grassland, farmland, town, wetland, and woodland) at Fuyang Airport and its surrounding areas, with the diversity indices in different seasons and different habitats analyzed. A total of 122 avian species belonging to 15 orders and 40 families were recorded. At Fuyang Airport, the avian species number was significantly higher in summer and autumn than in winter and spring, the avian density was the highest in autumn, and the Shannon diversity index and Pielou evenness index were the highest in summer. Among the five habitats at the Airport and its surrounding areas, woodland had the greatest avian species number and density, and the woodland, wetland, and farmland had higher Shannon diversity index than grassland and town. The most dangerous avian species to the airplanes at Fuyang Airport were Passer montanus, Pycnonotus sinensis, Hirundo rustica, Columba livia f. domestica, Pica pica, Streptopelia chinensis, and Sturnus cineraceu.