**NOVEL FRONTIERS OF ADVANCED NEUROIMAGING**

http://dx.doi.org/10.5772/2558 Edited by Kostas N. Fountas

#### **Contributors**

Aylin Bican, İbrahim Bora, Bahattin Hakyemez, Eray Alper, Volkan Özkol, Oktay Algın, Peter Walla, Shannon Bosshard, Aimee Mavratzakis, Maria De La Iglesia-Vaya, Jose Molina-Mateo, Luis Marti-Bonmati, Mª Jose Escarti-Fabra, Ahmad Kanaan, Robert P Granacher, Jr, Patrizia Bisiacchi, Elias Casula, Vincenza Tarantino, Demis. Basso, Hiroyuki Kato, Hoan Tran, Howard Yonas, Claudio Irace, Jaak Panksepp, Gracian Garcia-Marti, Angel Alberich-Bayarri, Ioannis Tsougos, Evanthia Kousi, Eftychia Kapsalaki, Kostas N. Fountas

#### **© The Editor(s) and the Author(s) 2013**

The moral rights of the and the author(s) have been asserted.

All rights to the book as a whole are reserved by INTECH. The book as a whole (compilation) cannot be reproduced, distributed or used for commercial or non-commercial purposes without INTECH's written permission. Enquiries concerning the use of the book should be directed to INTECH rights and permissions department (permissions@intechopen.com).

Violations are liable to prosecution under the governing Copyright Law.

Individual chapters of this publication are distributed under the terms of the Creative Commons Attribution 3.0 Unported License which permits commercial use, distribution and reproduction of the individual chapters, provided the original author(s) and source publication are appropriately acknowledged. If so indicated, certain images may not be included under the Creative Commons license. In such cases users will need to obtain permission from the license holder to reproduce the material. More details and guidelines concerning content reuse and adaptation can be foundat http://www.intechopen.com/copyright-policy.html.

#### **Notice**

Statements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book.

First published in Croatia, 2013 by INTECH d.o.o. eBook (PDF) Published by IN TECH d.o.o. Place and year of publication of eBook (PDF): Rijeka, 2019. IntechOpen is the global imprint of IN TECH d.o.o. Printed in Croatia

Legal deposit, Croatia: National and University Library in Zagreb

Additional hard and PDF copies can be obtained from<EMAIL_ADDRESS>
Novel Frontiers of Advanced Neuroimaging Edited by Kostas N. Fountas p. cm. ISBN 978-953-51-0923-5 eBook (PDF) ISBN 978-953-51-7060-0


**Chapter 32**

*Biotechnological Applications of Biomass*

[35] Vyazovkin S, Burnham AK, Criado JM, Pérez-Maqueda LA, Popescu C, SbirrazzuoliN. ICTAC kinetics committee recommendations for performing kinetic computations on thermal analysis data. Thermochim

[36] Xu Y, Zhang Y, Zhang G, Guo Y, Zhang J, Li G. Pyrolysis characteristics and kinetics of two Chinese lowrank coals. J Therm Anal Calorim.

[37] Xu Y, Zhang Y, Zhang G, Guo Y. Low temperature pyrolysates distribution and kinetics of Zhaotong lignite. Energy

Convers Manage. 2016;114:11-19

[40] Onsree T, Tippayawong N, Williams T, McCullough K, Barrow E, Pogaku R, Lauterbach J. Torrefaction of pelletized corn residues with wet flue gas. Bioresour Technol.

[41] Li SX, Chen CZ, Li MF, Xiao X. Torrefaction of corncob to produce charcoal under nitrogen and carbon dioxide atmospheres. Bioresour Technol.

[38] Chen WH, Peng J, Bi XT. A stateof-art review of biomass torrefaction, densification and applications,

RenewSust Energ Rev. 2015;44:847-866

[39] Prins MJ, Ptasinski KJ, Janssen FJJG. Torrefaction of wood, Part 1. Weight loss kinetics J. Anal. Appl. Pyrolysis.

Acta. 2011;520:1-19.

2015;122:975-84.

2006;77:28-34

2019;285:1213302

2018;249:348-353

[34] Funke A, Ziegler F. Hydrothermal carbonization of biomass: a summary and discussion of chemical mechanisms for process engineering. Biofuels, Bioprod Biorefin. 2010;4:160-177

**606**


*Edited by Bankole Fasanya*

This book provides workers and individuals with knowledge on the effective ways to understand the importance of human health and safety in workplaces. Workplace incident scenarios and research findings on human health and safety that could be an ideal information source for university students and workers are detailed in the book. Knowledge made available includes:

	- Social support and job satisfaction relationship at workplaces.
	- Recommendations to enhance good handwashing practices.
		- Worker's Act impacts on health and safety practices.
			- Good hygiene practices at public places.

Its comprehensive scope, along with its quick understanding, makes this book a handy working reference for good health and safety practices at workplaces.

Published in London, UK © 2020 IntechOpen © alekleks / iStock

Safety and Health for Workers - Research and Practical Perspective

Safety and Health

for Workers

Research and Practical Perspective

*Edited by Bankole Fasanya*


**4. Mechanism of resistance to targeted therapies**

Large advances in treatment results achieved with targeted therapies in mRCC are remarkable, but still between a third and two-thirds of patients with mRCC have tumors refractory to anti-VEGF and mTOR inhibitors from the beginning of treatment and all patients develop drug resistance and relapse some time during the course of their disease. Research of the mecha‐ nisms of resistance is very important in planning the development of new targeted agents [3, 23,24]. Most of information about drug resistance in mRCC known today is from the preclinical studies or studies on patients with different types of cancer, where targeted therapies are being in clinical practice for longer time (e.g. breast cancer). This is partially due to the rapid approval of targeted agents in mRCC which surpassed understanding of the mechanisms of response and resistance [3].

Until now two types of resistance to targeted therapy have been determined, so called intrinsic and extrinsic resistance [3].

to anti-VEGF antibody were associated with increase in infiltrating CD11b + GR1 + myeloid

Changing Mechanisms of Action as a Strategy for Sequential Targeted Therapy of Metastatic Renal-Cell Carcinoma

http://dx.doi.org/10.5772/55694

195

The proposed mechanisms of resistance to inhibitors of mammalian target of rapamycin (mTOR) include the presence of redundant signaling pathways, presence of KRAS or BRAF mutations, loss of phosphatase and tension homologue deleted on chromosome ten (PTEN),

Intrinsic resistance to anti-angiogenic factors and mTOR inhibitors is widespread and leads to poor patient outcome. Alternative pathways should be considered in this patients such as targeting RAF and MEK or PI3K/AKT. Including patients with resistant tumors in clinical trials

All patients who initially have clinical benefit of targeted therapy eventually develop resistance to it and experience disease progression. This resistance, named extrinsic resist‐ ance (also known as secondary, evasive, acquired or adaptive resistance) has been ex‐ plained more in detail [23]. TKI and VEGF inhibitors both target components of VEGF signaling pathway. Thus the mechanisms involved will affect any of these targeted agents. Extrinsic resistance results from the acquisition of adaptive mechanisms to the action of angiogenesis inhibitors which ultimately results in evasion of the angiogenesis and reemer‐

Sprouting of new vessels has been detected in Xenograft RCC tumors resected shortly after the start of sunitinib. The development of resistance is constantly preceded by restoration of blood flow, which suggests that new vasculature is less dependent (but not necessary inde‐

Different pro-angiogenic factors involved in the mechanism of resistance to targeted agents have been recognized. In a mouse model of pancreatic neuroendocrine cancer, resistant tumors expressed high levels of FGF 1, 2, ephrin A1, angiopoetin and interleukin-8 [23,25]. Inhibition

Interleukin-8 (IL-8) is a potent pro-angiogenic factor. Up-regulation of IL-8 plays an important role in RCC resistance. In a xenograft model of RCC mimicking clinical resistance to sunitinib, increased IL-8 secretion from tumors was associated with reactivation of tumor angiogenesis and administration of IL-8 neutralizing antibody lead to re-sensitization to sunitinib. Elevated IL-8 expression was also found in patients with tumors who did not respond to sunitinib from the beginning [5,22]. IL-angiogenic signaling may functionally compensate for the inhibition

Angiopoetin 2 (Ang-2) is a plasma glycoprotein involved in angiogenesis and cancer neovas‐ cularization. It is thought to have a role in development of the resistance. Levels of Ang-2 decrease after the initiation of sunitinib treatment and increase after the resistance occurs [23].

of these proteins was shown to inhibit tumor growth of resistant RCC-s [25].

testing these new agents that target these pathways is strongly recommended [23].

cells, which expressed several pro-angiogenic factors [23].

**4.2. Extrinsic resistance**

pendent) of VEGF [25].

gence of tumor-related vasculature [3,25].

*4.2.1. Up-regulation of pro-angiogenic factors*

of VEGF/VEGFR-mediated angiogenesis [5].

low cellular levels of p27 or 4E-bp1 and overexpression of eIF4E [3].

**Table 2.** Phase III trials of targeted agents in mRCC

#### **4.1. Intrinsic resistance**

Intrinsic resistance (primary resistance) occurs when tumor does not respond to the targeted therapy from the beginning of the treatment. Lack of the clinical benefit, even a short-lasting one is observed in these patients. Roughly 25% of patients are resistant to therapy; no response is detected on first evaluation after 2-3 months [23]. This type of resistance has not been explained entirely jet.

In the case of the resistance to VEGF inhibitors and TKI-s pre-existing pro-angiogenic factors, such as fibroblast growth factor-2 promote tumor angiogenesis. Pre-existence of pro-angio‐ genic factors compensate for the inhibition of VEGF signaling and thus allow angiogenesis to continue [3,23]. Pre-existing inflammatory cells may also contribute to the angiogenesis by expressing pro-angiogenic factors. In pre-clinical trials mRCC tumors that were not responsive to anti-VEGF antibody were associated with increase in infiltrating CD11b + GR1 + myeloid cells, which expressed several pro-angiogenic factors [23].

The proposed mechanisms of resistance to inhibitors of mammalian target of rapamycin (mTOR) include the presence of redundant signaling pathways, presence of KRAS or BRAF mutations, loss of phosphatase and tension homologue deleted on chromosome ten (PTEN), low cellular levels of p27 or 4E-bp1 and overexpression of eIF4E [3].

Intrinsic resistance to anti-angiogenic factors and mTOR inhibitors is widespread and leads to poor patient outcome. Alternative pathways should be considered in this patients such as targeting RAF and MEK or PI3K/AKT. Including patients with resistant tumors in clinical trials testing these new agents that target these pathways is strongly recommended [23].

### **4.2. Extrinsic resistance**

All patients who initially have clinical benefit of targeted therapy eventually develop resistance to it and experience disease progression. This resistance, named extrinsic resist‐ ance (also known as secondary, evasive, acquired or adaptive resistance) has been ex‐ plained more in detail [23]. TKI and VEGF inhibitors both target components of VEGF signaling pathway. Thus the mechanisms involved will affect any of these targeted agents. Extrinsic resistance results from the acquisition of adaptive mechanisms to the action of angiogenesis inhibitors which ultimately results in evasion of the angiogenesis and reemer‐ gence of tumor-related vasculature [3,25].

Sprouting of new vessels has been detected in Xenograft RCC tumors resected shortly after the start of sunitinib. The development of resistance is constantly preceded by restoration of blood flow, which suggests that new vasculature is less dependent (but not necessary inde‐ pendent) of VEGF [25].

### *4.2.1. Up-regulation of pro-angiogenic factors*

**4.1. Intrinsic resistance**

**Objective Response Rate**

31% Sunitinib 6% IFN

3% Placebo

31% Bev+IFN 13% Placebo+IFN

10% Sorafenib 2% Placebo

19% Axitinib 9% Sorafenib

1% Everolimus 0% Placebo

8.6% Tem 4.8% IFN 8.1% Tem+IFN

**Table 2.**

Intrinsic resistance (primary resistance) occurs when tumor does not respond to the targeted therapy from the beginning of the treatment. Lack of the clinical benefit, even a short-lasting one is observed in these patients. Roughly 25% of patients are resistant to therapy; no response is detected on first evaluation after 2-3 months [23]. This type of resistance has not been

In the case of the resistance to VEGF inhibitors and TKI-s pre-existing pro-angiogenic factors, such as fibroblast growth factor-2 promote tumor angiogenesis. Pre-existence of pro-angio‐ genic factors compensate for the inhibition of VEGF signaling and thus allow angiogenesis to continue [3,23]. Pre-existing inflammatory cells may also contribute to the angiogenesis by expressing pro-angiogenic factors. In pre-clinical trials mRCC tumors that were not responsive

Different pro-angiogenic factors involved in the mechanism of resistance to targeted agents have been recognized. In a mouse model of pancreatic neuroendocrine cancer, resistant tumors expressed high levels of FGF 1, 2, ephrin A1, angiopoetin and interleukin-8 [23,25]. Inhibition of these proteins was shown to inhibit tumor growth of resistant RCC-s [25].

Interleukin-8 (IL-8) is a potent pro-angiogenic factor. Up-regulation of IL-8 plays an important role in RCC resistance. In a xenograft model of RCC mimicking clinical resistance to sunitinib, increased IL-8 secretion from tumors was associated with reactivation of tumor angiogenesis and administration of IL-8 neutralizing antibody lead to re-sensitization to sunitinib. Elevated IL-8 expression was also found in patients with tumors who did not respond to sunitinib from the beginning [5,22]. IL-angiogenic signaling may functionally compensate for the inhibition of VEGF/VEGFR-mediated angiogenesis [5].

Angiopoetin 2 (Ang-2) is a plasma glycoprotein involved in angiogenesis and cancer neovas‐ cularization. It is thought to have a role in development of the resistance. Levels of Ang-2 decrease after the initiation of sunitinib treatment and increase after the resistance occurs [23]. Sphingosine kinase (S1P) is also supposed to play a role in the resistance. S1P is an enzyme that catalyzes the formation of sphingosine-1-phosphate which is associated with cell prolif‐ eration, survival and angiogenesis. Plasma levels of S1P decrease after the start of sunitinib treatment and increase again upon the development of resistance. In pre-clinical models administering neutralizing antibodies against S1P to mice, delayed the growth of sunitinibresistant tumors [23].

concluded that reversible changes in gene expression within the tumor cells and/or their microenvironment could be the possible mechanism of reversible resistance. He implanted sorafenib-resistant RCC into mice and after implantation tumors regained the sensitivity to

Changing Mechanisms of Action as a Strategy for Sequential Targeted Therapy of Metastatic Renal-Cell Carcinoma

http://dx.doi.org/10.5772/55694

197

In the case of sunitinib, the proposed mechanism of resistance is the activation or up-regulation of alternative angiogenic signals (e.g. FGF-s, ephrins, andiopoetins) while in the case of sorafenib this mechanism seem to be recruitment of pro-angiogenic bone marrow-derived cells and monocytes. Recruitment of perycites that help to maintain vessels permeable and func‐ tional and prevent endothelial cells from being affected by antiangiogenic therapies, is the proposed mechanisms of resistance to pasopanib. In the case of bevacisumab resistance the increased potential of tumor cells to invade without the need of neovascularization is supposed

Overcoming the resistance to first line therapy is one of the aims of administering the second line and beyond. Several factors play important role in selection of second line strategy: clinical

Sequential use of targeted agents is currently the standard of care for mRCC patients. This approach enables patients to get most benefit from these agents avoiding the excessive toxicity associated with combination therapy [26-28]. Targeted agent in the second line can have the same or different mechanism of action as first-line one. Limited data suggest that the use of a TKI after the failure of another TKI is reasonable and that there is not complete cross-resistance of these agents. The hypothesis behind this is that although TKIs share the same mechanism of action, their molecular targets are different. Despite this, the evidence of this approach is not strong; prospective, phase III trials are missing. Changing mechanism of action can have several advantages: greater chance of overcoming resistance while decreasing the probability of cumulative toxicity [4,25]. Toxicities of TKI-s and mTOR inhibitors for example, differ considerably. Frequent grade 3 toxicities encountered in patients on TKI-s are hand-foot syndrome, diarrhoea, fatigue, hypertension, neutropenia and leukopenia, while grade 3 toxicities in patients treated with mTOR inhibitors are rash, stomatitis, pneumonitis, anemia

The almost historical treatment strategy where changing of mechanism of action proved to be effective was TKI-s following cytokines. Currently this approach is not of clinical use anymore, because most of the patients get molecular targeted agent in the first line; however it is likely that some patients will have been treated with a cytokine previously. Phase III trials demon‐

sorafenib [4,25].

to be the mechanism [4,9,25].

and infection [25-30].

**5.1. TKI-s following cytokine therapy**

**5. Overcoming the resistance**

*4.2.7. Mechanism of resistance to different targeted agents*

evidence, toxicity issues and individual patient profile [4,25,26].

### *4.2.2. Down-regulation of angiostatic factors*

Down-regulation of angiostatic factors is another mechanism of resistance to TKI-s. Treatment with sunitinib and sorafenib results in the increased expression of several IFN-inducible genes including the angiostatic chemokines CXCL 10 and CXCL 11 and tumor suppressor genes. Following the development of resistance, the expression of IFN-γ and several of IFN-inducible genes is reduced. Down regulation of these factors is associated with the development of resistance to sunitinib and sorafenib [23].

### *4.2.3. Recruitment of bone marrow-derived cells*

Recruitment of bone marrow-derived cells which can result in the development of new blood vessels is another possible mechanism of resistance. In pre-clinical studies recruitment of CD11b + GR1 + myeloid cells cells resulted in resistance development. There is also evidence that tumor vasculature can be protected from anti-angiogenic therapy by increased pericyte coverage [23].

### *4.2.4. Development of invasion without angiogenesis*

Invasion of tumor in normal tissue and recruitment of normal tissue vasculature protect the tumors from anti-angiogenic therapy. It has been reported that the tumor of a patient experi‐ encing disease progression during antiangiogenic therapy had invaded the surrounding tissue and there had been increase of the vascularization from the normal tissue to the center of the tumor [23].

### *4.2.5. Resistance to m-TOR inhibitors*

Resistance to mTOR inhibitors is far less explained. It is supposed to be the result of activation of feedback loops that promote the activation of molecular signaling pathways of survival, increased activity of mTOR-complex 2, up-regulation of insulin-like growth factor and increase in the ERK/MAPK pathway signaling [4,24,25].

### *4.2.6. Reversible resistance*

Preclinical studies revealed that resistance to VEGF targeted therapies can be reversible. Hammers and colleagues grafted skin metastases of mRCC patient who had become resistant to sunitinib into mice and these xenogafts regained sensitivity and responded to sunitinib. Histology of original skin metastasis and xenograft revealed that a reversible epithelial-tomesenchymal transition could be responsible for acquired resistance to sunitinib. Zhang concluded that reversible changes in gene expression within the tumor cells and/or their microenvironment could be the possible mechanism of reversible resistance. He implanted sorafenib-resistant RCC into mice and after implantation tumors regained the sensitivity to sorafenib [4,25].

### *4.2.7. Mechanism of resistance to different targeted agents*

In the case of sunitinib, the proposed mechanism of resistance is the activation or up-regulation of alternative angiogenic signals (e.g. FGF-s, ephrins, andiopoetins) while in the case of sorafenib this mechanism seem to be recruitment of pro-angiogenic bone marrow-derived cells and monocytes. Recruitment of perycites that help to maintain vessels permeable and func‐ tional and prevent endothelial cells from being affected by antiangiogenic therapies, is the proposed mechanisms of resistance to pasopanib. In the case of bevacisumab resistance the increased potential of tumor cells to invade without the need of neovascularization is supposed to be the mechanism [4,9,25].


**2. Corruption: the slippery concept**

A definition of corruption is difficult to construct and universalise because of variable perceptions of what constitutes an unacceptable and selfish act across geographical space and across cultures and longitudinally over time. To help my argument, I will take you to these search results over the Internet, which is a global phenomenon. A search on the meaning of corruption raised the following:

I further looked for synonyms of corruption using the following constructs: immorality, lustful behaviour, distortion, vice and misrepresentation. The Internet gave the following:

I will end here otherwise I could show other results from other sources. The search results communicate to us that there are different ways of seeing, assessing and reacting to the same thing (corruption) depending on time and space and moods. Effectively we can say the quintessence of corruption is historically conditioned in space and time. What remains as core to a conceptualisation of corruption is the selfishness, the selfaggrandisement and undesirability of the deed and the undesirable consequences of corruption on the innocent person(s). If a hard, cut-and-dried definition of corruption is not achievable, we can still read through and accept the characterisation of corruption as a false, absurd, distorted (mis)representation of something, an act of immorality or sacrilege, unacceptable and abnormal lustful behaviour driven by greed and selfishness.


**Exploring the Role of Social Media in Health Promotion**

Special Issue Editors

**Michael Stellefson J. Don Chaney Beth H. Chaney Samantha R. Paige**

MDPI • Basel • Beijing • Wuhan • Barcelona • Belgrade • Manchester • Tokyo • Cluj • Tianjin

*Special Issue Editors* Michael Stellefson East Carolina University USA Samantha R. Paige University of Florida USA

J. Don Chaney East Carolina University USA

Beth H. Chaney East Carolina University USA

*Editorial Office* MDPI St. Alban-Anlage 66 4052 Basel, Switzerland

This is a reprint of articles from the Special Issue published online in the open access journal *International Journal of Environmental Research and Public Health* (ISSN 1660-4601) (available at: https: //www.mdpi.com/journal/ijerph/special issues/media health).

For citation purposes, cite each article independently as indicated on the article page online and as indicated below:

LastName, A.A.; LastName, B.B.; LastName, C.C. Article Title. *Journal Name* **Year**, *Article Number*, Page Range.

**ISBN 978-3-03936-328-5 (Pbk) ISBN 978-3-03936-329-2 (PDF)**

c 2020 by the authors. Articles in this book are Open Access and distributed under the Creative Commons Attribution (CC BY) license, which allows users to download, copy and build upon published articles, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications.

The book as a whole is distributed by MDPI under the terms and conditions of the Creative Commons license CC BY-NC-ND.

## **Contents**

## **Trevor Bopp and Michael Stellefson**

Practical and Ethical Considerations for Schools Using Social Media to Promote Physical Literacy in Youth Reprinted from: *Int. J. Environ. Res. Public Health* **2020**, *17*, 1225, doi:10.3390/ijerph17041225 . . . **137**

## **Nikol Kvardova, Hana Machackova and David Smahel**

The Direct and Indirect Effects of Online Social Support, Neuroticism, and Web Content Internalization on the Drive for Thinness among Women Visiting Health-Oriented Websites Reprinted from: *Int. J. Environ. Res. Public Health* **2020**, *17*, 2416, doi:10.3390/ijerph17072416 . . . **147**

## **Michael Stellefson, Samantha R. Paige, Beth H. Chaney and J. Don Chaney**

Evolving Role of Social Media in Health Promotion: Updated Responsibilities for Health Education Specialists

Reprinted from: *Int. J. Environ. Res. Public Health* **2020**, *17*, 1153, doi:10.3390/ijerph17041153 . . . **161**


**5. Conclusion**

Over the last decades, there have been revolutionary developments in mechanical support. Although patients with chronic heart failure exhibit improved survivorship with the application of evidence-based medical therapies, VADs are superior to medical therapy for improving survival among patients with advanced heart failure with reduced ejection fraction [18]. This topic is important because estimates reveal that over 18 million persons are diagnosed with heart failure in the United States and Europe at present [17]. Furthermore, heart failure is far more prevalent in older age groups, reaching 4.3% among persons aged 65–70 years in 2012, and is projected to increase steadily, reaching 8.5% in the US by the year 2030 [17].

For individuals with refractory heart failure requiring transplantation, it has been estimated that a VAD is used as a bridge to transplantation in approximately 9% of children and 25% of adult patients The shortage of donor organs and the expanding pool of patients with heart failure have led to growing interest in mechanical circulatory support; fortunately, we have observed meaningful and positive trends from the incorporation of MCS over the past five decades. We commend all those individuals who have been at the forefront of these developments and equally acknowledge those with behind-the-scenes contributions to this field.

As of today, this modality has been successfully expanded to employ MCS as bridge-to-transplant, bridge-to-recuperation, or destination therapy. However, following the withdrawal of HVAD from the global market in June of 2021, we are currently left with a reduced armamentarium for managing patients with advanced heart failure with reduced ejection fraction, particularly in the pediatric population. Therefore, shifting the paradigm to advance device miniaturization, improving surgical implantation techniques, and effectively reducing adverse events would be of greatest value in the following decades to further advance the field of mechanical circulation. An integrative alliance among technology companies, healthcare practitioners, and researchers is paramount to promoting education, innovation, and accessibility.


**5. Conclusions**

Scientists are looking at every possible cure for the virus, and modern technology increasingly searches for a possible cure. It is pertinent that technology has become part of our everyday lives; it has additionally now been used in the fight against the coronavirus. This paper highlights the problem of the coronavirus and discusses some algorithms that are practically used in hospitals. The paper also discusses the fact that there is an interest in building a yardstick framework to examine the present methods. The present systems have

precise correctness in predicting COVID-19 symptoms with various types of pneumonia using X-rays scans; however, they do not have both interpretability and transparency. Therefore, we can conclude that technology has many capabilities to overcome the medical and social problems caused by the COVID-19 pandemic. Few such capabilities are advanced and adequate for demonstrating any impact. CT investigation performs a vital function in the mitigation of COVID-19. It was used at the initial detection of the COVID-19 virus, particularly in the extremely vulnerable, asymptomatic occurrences with non-positive PCR tests; CT may perform functions in the following points: triage of patients, estimation of deteriorating, estimation of good cure, and problem handle. The triage of patients can be divided into three categories: possibly with COVID-19, without COVID-19, and seriousness of the infection.

**Author Contributions:** Conceptualization, K.H.A. and A.M.H.; methodology, L.A., A.M.H. and S.K.M.A.; investigation, E.H.M. and B.O.G.; resources, K.H.A. and A.M.H.; writing—original draft preparation, A.M.H. and S.K.M.A.; writing—review and editing, A.M.H.; project administration, K.H.A.; funding acquisition, K.H.A.; writing—review and editing A.H.G. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by the Deanship of Scientific Research at Umm Al-Qura University (https://uqu.edu.sa) for supporting this work by grant code: (22UQU4320277DS15) to KA. The authors would like to thank the Deanship of Scientific Research at Umm Al-Qura University for supporting this work.

**Institutional Review Board Statement:** Not applicable.

**Informed Consent Statement:** Not applicable.

**Data Availability Statement:** Not applicable.

**Conflicts of Interest:** The authors declare no conflict of interest.