Covid-19 Detection For CT-scan Images Using Transfer Learning Models

COVID-19 is a respiratory illness caused by a virus called SARS-CoV-2 which affected around 455 million people around the world. CT-scan is a medical imaging technique that uses X-rays to create detailed images of the body and which can be used to detect many respiratory diseases. Transfer learning models are a type of machine learning model that are trained on a large dataset of images and which can be used for their already trained ability to extract features from image in other tasks. They can then be used to classify new images with similar features.This paper presents a study of different transfer learning models for the task of classifying chest X-ray images into three classes: COVID-19, pneumonia, and normal. The study was implemented using Python and the dataset used was the COVID-19 Chest X-ray Dataset. The train-test split used was 0.2–0.8. The parameters used to test the models were the precision, recall, accuracy, F1 score, and Matthew’s correlation score. Other than these, different optimizers were also compared such as ADAM, SGD with different learning rates of 0.01, 0.001, and 0.0001.The models used in this study are EfficientNetB0, EfficientNetB7, VGG16, and InceptionV3. Out of these models, the most effective model was the EfficientNetB0 model, which achieved an accuracy of 98.6%. This study provides valuable insights into the use of transfer learning for medical image analysis. The results suggest that transfer learning can be used to develop accurate and efficient models that can be used as a secondary option for the diagnosis of COVID-19 using chest X-ray images

Radiological examination of impact of edentulism on the articular eminence inclination using orthopantomogram

Background: Occlusion is an important component of the temporomandibular joint (TMJ). Little is known about the association between missing teeth and TMJ changes. The objective of this study was to compare inclination of the articular eminence (AE) between dentulous and edentulous arch. Method: A total of 500 patients were divided into group A (dentulous) and group B (edentulous). Group B was further divided into subgroups based on years of edentulism into group 1, group 2 and group 3. On patient’s panoramic radiograph, the sagittal outline of the AE and glenoid fossa were traced, and a sagittal condylar path inclination was constructed by joining the crest of the glenoid fossa and the crest of AE. This was then related to the constructed Frankfurt’s horizontal plane to determine the inclination of AE. Results: The mean measured value for the AE inclination was varying with all the groups. The mean and standard deviation value (combining right & left) for Group A was 42.8+/-6.83 degrees, Group B was 30.45+/-6.55degrees, Group 1 was 30.2+/-7.23degrees, Group 2 was 31.2+/-4.75 degrees, and Group 3 was 27.5+/-9.3 degrees. Significant differences were found in AE inclination between the dentulous and edentulous groups (P <0.05). Conclusion: A significant difference in the AE inclination was found between dentulous and edentulous groups as well as with increase in the period of edentulism

Harnessing Radiation Biology to Augment Immunotherapy for Glioblastoma

Glioblastoma is the most common adult primary brain tumor and carries a dismal prognosis. Radiation is a standard first-line therapy, typically deployed following maximal safe surgical debulking, when possible, in combination with cytotoxic chemotherapy. For other systemic cancers, standard of care is being transformed by immunotherapies, including checkpoint-blocking antibodies targeting CTLA-4 and PD-1/PD-L1, with potential for long-term remission. Ongoing studies are evaluating the role of immunotherapies for GBM. Despite dramatic responses in some cases, randomized trials to date have not met primary outcomes. Challenges have been attributed in part to the immunologically “cold” nature of glioblastoma relative to other malignancies successfully treated with immunotherapy. Radiation may serve as a mechanism to improve tumor immunogenicity. In this review, we critically evaluate current evidence regarding radiation as a synergistic facilitator of immunotherapies through modulation of both the innate and adaptive immune milieu. Although current preclinical data encourage efforts to harness synergistic biology between radiation and immunotherapy, several practical and scientific challenges remain. Moreover, insights from radiation biology may unveil additional novel opportunities to help mobilize immunity against GBM

Harnessing the Power of Onco-Immunotherapy with Checkpoint Inhibitors

Oncolytic viruses represent a diverse class of replication competent viruses that curtail tumor growth. These viruses, through their natural ability or through genetic modifications, can selectively replicate within tumor cells and induce cell death while leaving normal cells intact. Apart from the direct oncolytic activity, these viruses mediate tumor cell death via the induction of innate and adaptive immune responses. The field of oncolytic viruses has seen substantial advancement with the progression of numerous oncolytic viruses in various phases of clinical trials. Tumors employ a plethora of mechanisms to establish growth and subsequently metastasize. These include evasion of immune surveillance by inducing up-regulation of checkpoint proteins which function to abrogate T cell effector functions. Currently, antibodies blocking checkpoint proteins such as anti-cytotoxic T-lymphocyte antigen-4 (CTLA-4) and anti-programmed cell death-1 (PD-1) have been approved to treat cancer and shown to impart durable clinical responses. These antibodies typically need pre-existing active immune tumor microenvironment to establish durable clinical outcomes and not every patient responds to these therapies. This review provides an overview of published pre-clinical studies demonstrating superior therapeutic efficacy of combining oncolytic viruses with checkpoint blockade compared to monotherapies. These studies provide compelling evidence that oncolytic therapy can be potentiated by coupling it with checkpoint therapies

Complexes of Vesicular Stomatitis Virus Matrix Protein with Host Rae1 and Nup98 Involved in Inhibition of Host Transcription

<div><p>Vesicular stomatitis virus (VSV) suppresses antiviral responses in infected cells by inhibiting host gene expression at multiple levels, including transcription, nuclear cytoplasmic transport, and translation. The inhibition of host gene expression is due to the activity of the viral matrix (M) protein. Previous studies have shown that M protein interacts with host proteins Rae1 and Nup98 that have been implicated in regulating nuclear-cytoplasmic transport. However, Rae1 function is not essential for host mRNA transport, raising the question of how interaction of a viral protein with a host protein that is not essential for gene expression causes a global inhibition at multiple levels. We tested the hypothesis that there may be multiple M protein-Rae1 complexes involved in inhibiting host gene expression at multiple levels. Using size exclusion chromatography and sedimentation velocity analysis, it was determined that Rae1 exists in high, intermediate, and low molecular weight complexes. The intermediate molecular weight complexes containing Nup98 interacted most efficiently with M protein. The low molecular weight form also interacted with M protein in cells that overexpress Rae1 or cells in which Nup98 expression was silenced. Silencing Rae1 expression had little if any effect on nuclear accumulation of host mRNA in VSV-infected cells, nor did it affect VSV's ability to inhibit host translation. Instead, silencing Rae1 expression reduced the ability of VSV to inhibit host transcription. M protein interacted efficiently with Rae1-Nup98 complexes associated with the chromatin fraction of host nuclei, consistent with an effect on host transcription. These results support the idea that M protein-Rae1 complexes serve as platforms to promote the interaction of M protein with other factors involved in host transcription. They also support the idea that Rae1-Nup98 complexes play a previously under-appreciated role in regulation of transcription.</p> </div

Effect of silencing Rae1 or Nup98 expression on RNA synthesis in VSV-infected cells.

<p>HeLa cells transfected with the indicated siRNA were either mock-infected or infected with VSV in the presence or absence of actinomycin D. At 6 h postinfection, cells were labeled with ³H uridine for 30 min; RNA was acid-precipitated, and radioactivity was determined by scintillation counting. Data shown are mean ± s.d. for triplicate cultures from a representative experiment.</p>a<p>Abbreviations: ActD - actinomycin D; NT – non-targeting siRNA.</p

Effects of silencing the expression of Rae1 or Nup98 on host and viral transcription in VSV-infected cells.

<p>HeLa cells were either not transfected or transfected with Rae1 siRNA (<b>A</b>), Nup98 siRNA (<b>B</b>) or non-targeting (NT) siRNA. At 72 hours post-transfection, cells were either mock or infected with recombinant wild-type (rwt) virus for 6 hours in the presence or absence of actinomycin D (ActD, 5 µg/ml). Cells were labeled with [³H] uridine for 30 minutes. Cells were lysed and RNA was precipitated using trichloroacetic acid, and acid precipitable radioactivity was measured. The graph represents host (ActD sensitive) and viral (ActD insensitive) RNA synthesis expressed as a percentage of total RNA synthesis in mock infected cells as illustrated in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1002929#ppat-1002929-t001" target="_blank">Table 1</a>. The data shown are means ± standard deviation from five independent experiments.</p

Gel filtration and sedimentation velocity analysis of complexes containing Rae1.

<p>(<b>A</b>) Cell lysates were chromatographed on a Superdex 200 column. Fractions were analyzed by immunoblots probed for Rae1 and Nup98. Arrows represent the fractions where standards of the indicated molecular weight eluted under the same conditions. The graph represents quantification of % Rae1 in each fraction normalized to total Rae1 eluting in all fractions. Vo indicates the void volume. (<b>B</b>) Column fractions from the same experiment as in (<b>A</b>) were incubated with wt GST-M protein (M) or GST (G) on glutathione beads for 1 hour. Bound fractions were analyzed by immunoblots probed for Rae1 and Nup98. (<b>C</b>) Cells were transfected with plasmid DNA encoding HA-Rae1. Lysates were chromatographed on a Superdex 200 column. Fractions were analyzed by immunoblots probed for HA. (<b>D</b>) Column fractions from (<b>C</b>) were incubated with wt GST-M protein (M) or GST (G) on glutathione beads for 1 hour. Bound fractions were analyzed by immunoblots probed for HA. (<b>E</b>) Cell lysates were subjected to sucrose gradient centrifugation. Fractions were collected from the top and probed for Rae1 (top panel) and Nup98 (bottom panel). Arrows represent fractions containing standards with the indicated s_20,w value subjected to the same conditions. (<b>F</b>) Sucrose gradient fractions from (<b>E</b>) were incubated with GST-M protein (M) or GST (G) on glutathione beads for 14 hours at 4°C. Bound fractions were analyzed by immunoblots probed for Rae1 and Nup98.</p