ABSTRACT
Objective: To develop an automated landmark location system applicable to the case of landmark missing. Methods: Four and eighty-one lateral cephalograms, which contained 240 males and 241 females, with an average age of (24.5±5.6) years, taken from January 2015 to January 2021 in the Department of Orthodontics, Capital Medical University School of Stomatology, and met the inclusion criteria were collected. Five postgraduate orthodontic students were the annotators to manually locate 61 possible landmarks in 481 lateral cephalograms. Two assistant professors in the department as reviewers performed calibration. Two professors as arbitrators, made final decision. Data sets were established (341 were used as training set, 40 as validation set, and 100 as test set). In this paper, an automatic landmarks identification and location model based on convolutional neural networks (CNN), CephaNET, was developed. The model was trained by feeding the original image into the feature extraction module and convolutional pose machine (CPM) module to locate landmarks with high accuracy using deep supervision. Training set was enhanced to 1 684 images by histogram equalization, cropping, and adjustment of brightness. The model was trained to compare the Gaussian heat maps output from the network with the set threshold to identify landmark missing cases. Test set of 100 lateral cephalograms was used to test the accuracy of the model. The evaluation criteria used were success detection rate of missing landmark, mean radial error (MRE) and success detection rate (SDR) in the range of 2.0, 2.5, 3.0, 3.5 and 4.0 mm. Results: The model identified and located 61 commonly used landmarks in 0.13 seconds on average. It had an average accuracy of 93.5% in identifying missing landmarks. The MRE of our testing set was (1.19±0.91) mm. SDR of 2.0, 2.5, 3.0, 3.5 and 4.0 mm were 85.4%, 90.2%, 93.5%, 95.4%, 97.0% respectively. Conclusions: The model proposed in this paper could adapt to the absence of landmark in lateral cephalograms and locate 61 commonly used landmarks with high accuracy to meet the requirements of different cephalometric analysis methods.
Subject(s)
Neural Networks, Computer , Orthodontics , Male , Female , Humans , Adolescent , Young Adult , Adult , Reproducibility of Results , Cephalometry/methods , RadiographyABSTRACT
In an effort to identify the signal transduction mechanism associated with the inhibition of juvenile hormone (JH) biosynthesis by the neuropeptides allatostatins, levels of the cyclic nucleotides cAMP and cGMP were measured in corpora allata (CA) of virgin and mated Diploptera punctata females using radioimmunoassays. Treatment of isolated CA with varying concentrations of synthetic allatostatins 1, 2, 3 or 4 did not elicit significant changes in the levels of either cAMP or cGMP in any of the test glands, suggesting that these compounds do not act as second messengers for the four allatostatins tested. Simultaneous treatment of CA with allatostatin 4 and the adenylate cyclase activator forskolin did not increase the degree of inhibition of juvenile hormone biosynthesis relative to that obtained with forskolin (5 or 50 microM) alone. We interpret these results as lending further support to the suggestion that cyclic nucleotides do not play a role in the signal transduction of allatostatins 1-4 in cockroach CA.
Subject(s)
Cockroaches/physiology , Cyclic AMP/physiology , Cyclic GMP/physiology , Juvenile Hormones/biosynthesis , Neuropeptides/pharmacology , Second Messenger Systems/drug effects , Animals , Cockroaches/drug effects , Colforsin/pharmacology , Corpora Allata/drug effects , Corpora Allata/metabolism , Cyclic AMP/analysis , Cyclic GMP/analysis , Depression, Chemical , Female , Sexual Behavior, AnimalABSTRACT
The lymphocytes isolated from perfused or non-perfused circulations before, during, and after hyperthermic isolated limb perfusion (HILP) in the four patients with malignant melanoma were analysed for the expression of CD54 (ICAM-1), CD58 (LFA-3), CD4, CD8, HLA class I and class II in order to investigate the mechanism(s) of the activation of such immunocompetent cells as natural killer (NK)-cells or T-lymphocytes by HILP. It was thus found that the lymphocyte populations expressing CD54 increased significantly 1 day after HILP in the four patients examined. The lymphocyte populations expressing CD58 apparently increased. It was also found that the NK-cell and T-lymphocyte activities increased during or after HILP in the present four cases as observed previously in the other melanoma patients. These results indicate that our HILP system may augment the immunological activities through the mechanisms of the induction of CD54 or CD58 expression in the peripheral lymphocytes of the melanoma patients who receive HILP.
Subject(s)
Chemotherapy, Cancer, Regional Perfusion , Hyperthermia, Induced , Intercellular Adhesion Molecule-1/analysis , Lymphocytes/immunology , Melanoma/therapy , Skin Neoplasms/therapy , Adult , Aged , Extremities/blood supply , Female , Humans , Killer Cells, Natural/physiology , Male , Melanoma/immunology , Melanoma/pathology , Middle Aged , Skin Neoplasms/immunology , Skin Neoplasms/pathologyABSTRACT
The production of juvenile hormone III (JH III) by the corpora allata of the cockroach Diploptera punctata is regulated in part by peptides originating from the brain. One group of these peptides, termed allatostatins, reversibly inhibits the biosynthesis of JH in vitro. Allatostatin 4 (AST4: Asp-Arg-Leu-Tyr-Ser-Phe-Gly-Leu-amide) is the smallest member of the AST family yet defined and was used as the benchmark peptide for these initial structure-activity studies. Two initial analog series of AST4 were examined for the ability of each analog to inhibit JH biosynthesis by corpora allata in vitro. Each analog series consisted of analogs that contained a single amino acid change from the native AST4 sequence. The first series contained Ala replacement analogs and the second contained analogs with D-amino acid replacements. The first analog series used Ala replacements to help indicate which amino acid side chains were most important for inhibition of JH biosynthesis. The most important side chain appeared to be Leu8 followed by Phe6 and Tyr4. Additionally, the D-amino acid series suggested that a secondary structural element(s) at the C-terminus of AST4 could be important to the biological activity.
Subject(s)
Corpora Allata/drug effects , Corpora Allata/metabolism , Juvenile Hormones/biosynthesis , Neuropeptides/pharmacology , Amino Acid Sequence , Animals , Cockroaches , Female , Models, Molecular , Molecular Sequence Data , Neuropeptides/chemistry , Oligopeptides/chemistry , Oligopeptides/pharmacology , Protein Structure, Secondary , Stereoisomerism , Structure-Activity RelationshipABSTRACT
The expression of intercellular adhesion molecule-1 (ICAM-1) in mouse B16 and human melanoma cell lines was investigated by indirect immunofluorescence using a FACScan analyzer. Mouse B16 melanoma cell lines (B16-F1 and F10) did not express ICAM-1 under ordinary culture conditions. Neither in vitro hyperthermia at 41 degrees C for 3 or 6 hr nor cytokines such as gamma interferon (IFN-gamma) or tumor necrosis factor alpha (TNF-alpha) induced ICAM-1 expression in B16 melanoma cell lines. A combination of IFN-gamma with TNF-alpha caused slight induction of ICAM-1 expression in the B16-F10 melanoma cell line. Hyperthermia at 41 degrees C for 3 hr in combination with the cytokines induced a slight expression of ICAM-1 in the B16-F1 melanoma cell line. Hyperthermia at 41 degrees C for 3 hr or 6 hr did not induce de novo ICAM-1 expression but hyperthermia at 43 degrees C for 6 hr caused rather suppression of the expression of ICAM-1 in the three human melanoma cell lines tested. In contrast, they showed a clear increase in the expression of ICAM-1 after treatment with either with IFN-gamma or TNF-alpha, and the expression was further augmented by a combination of the two cytokines. Treatment with cytokines in combination with hyperthermia at 41 degrees C or 43 degrees C for 3 hr did not augment the expression of ICAM-1 over that in cytokine-treated human melanoma cell lines, at normal temperatures. Thus, it is concluded that mouse B16-F1 and F10 melanoma cell lines are different from human melanoma cell lines in terms of induction of ICAM-1 expression by cytokines and/or hyperthermia.
Subject(s)
Cytokines/pharmacology , Hot Temperature , Intercellular Adhesion Molecule-1/metabolism , Melanoma, Experimental/metabolism , Skin Neoplasms/metabolism , Animals , Flow Cytometry , Fluorescent Antibody Technique, Indirect , Humans , Interferon-gamma/pharmacology , Mice , Tumor Cells, Cultured/metabolism , Tumor Necrosis Factor-alpha/pharmacologyABSTRACT
We investigate the crossover behavior from two-dimensional (2D) to three-dimensional in multilayers of magnetic nanodots grown by stacking 2D Fe nanodot assemblies on Cu(111) single crystal substrate with a Cu spacing layer. Using an in situ magneto-optical Kerr effect, we have observed a striking ferromagnetic to spin-glass-like phase transition with an increasing number of Fe dot layers. The topmost layer of the Fe dots survives the phase transition and remains ferromagnetic. This unusual surface ferromagnetism is likely caused by a surface-state-mediated coupling which is stronger than the coupling in bulk layers. This is confirmed by the fact that the critical temperature of the surface ferromagnetism is considerably higher than that of the bulk spin-glass phase in the system.