Forest fire events for selected Assam State forests (2001–2011).
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"5907",leadTitle:null,fullTitle:"Stem Cells in Clinical Practice and Tissue Engineering",title:"Stem Cells in Clinical Practice and Tissue Engineering",subtitle:null,reviewType:"peer-reviewed",abstract:"Stem Cells in Clinical Practice and Tissue Engineering is a concise book on applied methods of stem cell differentiation and optimization using tissue engineering methods. 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\r\n\tThalassemia disease has stood the test of time and has persisted for thousands of years in humans. Global Disease Burden with Thalassemia still makes it one of the formidable inherited genetic noncommunicable diseases of concern which propagates in families due to lack of access to adequate genetic counseling facilities.
\r\n\r\n\tNew developments in the form of improvement in stem cell transplantation and medication approval in the developed world have shown promise and need to be updated to every clinician managing thalassemia.
\r\n\tBasic science studies have provided new insights into the pathophysiology of β-thalassemia. Studies of genotypic and phenotypic heterogeneity among patients and a better understanding of the control of erythropoiesis have provided new targets for designing novel agents that can be tailored to individual patient needs. JAK-2 kinase inhibitors and agents targeting the GDF-11/SMAD pathway are in clinical trials.
\r\n\tThis book will attempt to discuss the historical background of the disease and present the most up-to-date material regarding disease management in today's world for the reader to be updated on the best practice management of the disease.
",isbn:"978-1-83969-158-4",printIsbn:"978-1-83969-157-7",pdfIsbn:"978-1-83969-159-1",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"23abb2fecebc48a2df8a954eb8378930",bookSignature:"Dr. Akshat Jain",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10727.jpg",keywords:"History of Gene Mutation, Genetic Counselling, Anemia, Genotyping, Hemoglobin Electrophoresis, HLA typing, Hemolysis, Aplastic Anemia, Blood Transfusion, Laboratory Testing, Fetal Hemoglobin Modifiers, Gene Therapy",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 4th 2021",dateEndSecondStepPublish:"March 4th 2021",dateEndThirdStepPublish:"May 3rd 2021",dateEndFourthStepPublish:"July 22nd 2021",dateEndFifthStepPublish:"September 20th 2021",remainingDaysToSecondStep:"3 days",secondStepPassed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:"A board-certified pediatrician with a specialization in pediatric hematology-oncology and stem cell transplantation. In collaboration with Harvard Medical School, he studied and reported the outcomes of a global hemophilia collaboration. He is a member of the American Board of Pediatrics, Hematology, and American Board of Pediatrics, also he is a Committee member for the American Society of Pediatric Hematology-Oncology Special Interest Group in Global Pediatric Hematology oncology.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"344600",title:"Dr.",name:"Akshat",middleName:null,surname:"Jain",slug:"akshat-jain",fullName:"Akshat Jain",profilePictureURL:"https://mts.intechopen.com/storage/users/344600/images/system/344600.jpg",biography:"Akshat Jain M.D. M.P.H.\n11175 Campus Street \nLoma Linda, California 92354\nPhone: (917) 331-3216\nakshatjainusa@gmail.com \n\nMEDICAL EDUCATION \n●\tS.S.R. Medical College, Belle Rive, Mauritius - MBBS, Bachelor of Medicine Bachelor of Surgery, 2007\n●\tPediatrics Residency Training ,The New York Medical College, Metropolitan Hospital , Dec2008-Dec 2011\n●\tPediatric Hematology Oncology and Stem Cell Transplant Fellowship, Cohen’s Children's Hospital of New York at LIJ-North Shore Health system. July 2012- September 2015\n●\tMaster’s in Public Health ,Hofstra University School of Public Health ,New York , August 2015\n\n\nHONORS/ AWARDS \n●\tThe New York Academy of Medicine Honorary Associate Award , December 2009\n●\tProgram Leadership Award - Committee of Interns and Residents (C.I.R./SIEU), April 2010\n●\tAmerican Academy of Pediatrics Program Delegate Award, New York Medical College, December 2010.\n●\tCitation of Honor from New York County for Excellence in Medicine and Service to Long Island, New York,Nassau county executive chambers , August 15,2015 \n●\tTimes of India N.R.I. ( Non Resident Achiever ) award , August 2015 \n●\tCertificate for academic excellence –Hofstra University School of Health Science & Human Services, New York August 26, 2015\n●\tAmerican Society of Hematology Leadership Institute Award , April 2016\n●\tGlobal Health Speaker Award , convener of Global Health Symposium, Hofstra NorthWell School of Medicine and School of Public health , May 2016\n●\tInternational Pediatric Lymphoma Meeting ,Session Chairperson of Pediatric Lymphoma , Indian Society of Hematology and Oncology , November 2016\n●\tContent Leader Award for Hematology perspective’s in the Global CoronaVirus Pandemic Preparedness Response for Medical Association of physicians of Indian Origin, April 2020.\n●\tConvener and Chairperson International Webinar for COVID 19 Coagulopathy, May 2020. \n●\tFeatured in the Top Doctors magazine 2020, ranked top pediatric Hematologist Oncologist for Southern California.\n\nNATIONAL/INTERNATIONAL POSITIONS \n●\tHofstra University Dean Advisory Board for the School of Health Professions, December 2017\n●\tEditorial Board – American Society of Pediatric Hematology Oncology Communications Committee, International Journal of Hematology Research (ISSN 2409-3548)\n●\tReviewer - JAMA Pediatrics (ISSN: 2168-6203), British Medical Journal (ISSN, 1468-5833), JAMA Oncology (ISSN: 2374-2437), International Journal of Hematology Research (ISSN 2394—806X), Journal of Pediatric Hematology and Oncology (ISSN: 1536-3678), New England Journal of Medicine (Resident 360). \n●\tMember – Core committee: American Cancer Society (A.C.S.) and American Academy of Pediatrics (A.A.P.) - Joint global pediatric Oncology taskforce.\n●\tAdvisor -World Health Organization, South East Asia for maternal and child health initiatives.( 2013-Ongoing) , Ministry of Health and Family Welfare ,Government of India ( 2014- Ongoing ) , American Academy of Pediatrics &American Cancer Society Global Taskforce on Pediatric Cancers.( 2014-Ongoing )\n●\tEditor – AAPI journal (American Association of Physicians of Indian Origin. Circulation -40,000)\n●\tVisiting Professorship in Hematology Oncology and Stem Cell Transplantation, Rajasthan University of Medical Sciences, India. ( 2009-Ongoing )\n●\tIndustry Advisor – Bayer, UniQure, Sanofi-Genzyme, Takeda, CSL Behring\n●\tDirector of International Bone Marrow Failure Consortium- India, part of the Global Hematology Initiative of Cohen Children’s Medical Center, New York, August 2015-2017. \n●\tCommittee member for the American Society of Pediatric Hematology Oncology Special Interest Group in Global Pediatric Hematology oncology. ( 2016- Ongoing)\n\n\n WORK EXPERIENCE \nNov 2017- Current Loma Linda University Children’s Hospital \n Director Division of Pediatric Hematology \n Director, Comprehensive Hemophilia Program\n Director, Comprehensive Sickle Cell Program \n Division of Pediatric Hematology Oncology and Stem Cell Transplantation\n Professor of Public Health, Loma Linda University School of Public Health \n\nMar 2017– Oct 2017 Pediatrics and Pediatric Hematology Oncology Practice \n Adventist Health Ukiah Valley, California \n\nSept 2015 –Aug 2016 Assistant Professor Pediatrics, Hofstra North Shore LIJ School of Medicine \n Section Head –Global Pediatric Hematology Oncology and Stem Cell Transplantation\n North Shore LIJ Health system.\n Associate Adjunct Faculty, Hofstra University School of Public Health.\n\nJuly 2012 – Sep 2015 The Steven and Alexandra Cohen’s Children's’ Hospital of New York at LIJ-North Shore \n Hofstra University - Pediatrics Hematology Oncology and Stem Cell Transplant Fellowship \n Chief - Jeffrey Lipton MD\n\nDec 2011- April 2012 Global Health : SMS Medical College and Group of Hospitals, Government of India \n Project Director for Project A.G.N.I. - Set up a regional Lead Poisoning prevention and \n anemia nodal center \n \n Course Director - Pediatric Subspecialty training module for Pediatricians at J.K. Lone \n Children’s Hospital for Government of India. \n\nDec 08- Dec 2011 The New York Medical College, Residency in Pediatrics \n Metropolitan Hospital, NY\n Maria Fareri Children's Hospital at Westchester.\n The Memorial Sloan Kettering Hospital. NY\n House staff on Stem Cell Transplantation service.\n \nApril – August 2008 Oklahoma State Medical Association (O.S.M.A.) Externship Program\n The Integris Baptist Teaching Hospital and Nazih Zuhdi Transplant Center\n\nRESEARCH EXPERIENCE \nNov 2017 – Ongoing: Current and ongoing – Director, Inherited Bleeding Disorder Experimental Therapeutics Program, Loma Linda University School of Medicine\nJan 2014 –July 2015 - Hofstra University School of Public Health \n Needs Assessment to barriers in cancer care for newly diagnosed patients in a resource \n Limited setting. \n Principal Investigator - Akshat Jain, Co-PI -Corrine Kyriacou \n\nJune 2012- July 2015 - Steven and Alexandra Cohen Children’s Medical Center \n Study – Non Invasive assessment of endothelial dysfunction in children with Sickle cell \n Disease. \n Co-Principal Investigator – Banu Aygun MD\n Study – Multicenter study assessing outcome of Reduced Intensity Conditioning for \n patients undergoing hematopoetic stem cell transplantation for Sickle cell disease . \n Co-Principal Investigator – Indira Sahdev MD\n \nJan 2012- Mar12 A.G.N.I. (Anterograde Growth Normalization Initiative) \n Project Director, Project of Government of India for establishment of Universal Lead \n Independent Pilot project to study effects of Elevated Blood Lead levels in children \n suffering from Developmental disorders- Adapted by W.H.O. 2014 for a National Level \n Lead Screening program, India \n \nJan 2009- Dec11 The New York Medical College, Metropolitan Hospital Center. NY\n Resident Physician – Hypothalamic volumes in patients with Growth Hormone deficiency.\n Maria Fareri Children's hospital / Dr.Richard Noto - Pediatric Endocrinology\n \nApril 2008-Dec 08 Nazih Zuhdi Transplant Institute, Integris Baptist Hospital, Oklahoma City\n Project – Single institution outcome study for Solid organ transplants\n Research Assistant Department of Hepatology\n \nOct 2007 – Dec07 Mount Sinai School of Medicine, New York, NY\n Project- Arterio-venous fistula post liver transplantation.\n Research mentor-Dr. Charissa Chang, Assistant Professor in Department of Liver Diseases. \n\nCERTIFICATION\n\n1.\tCalifornia State Medical License 8/2016- Present , New York State Licensure 8/2013-12/16\n2.\tAmerican Board of Pediatrics - Board certified, 11/14- Present\n3.\tAmerican Board of Pediatric Hematology Oncology – Board Certified , 06/2018- Present\n4.\tNeonatal Advanced Life Support 06/2009-Present \n5.\tPediatric Advanced Life Support 06/2009-Present \n6.\tECFMG Certification 12/2007-Present \n\nORAL PRESENTATIONS \n\n\n1.\tLeukemia and Lymphoma Society of America C.M.E. Symposium presentation – Leukemia and Beyond: Advances in Cancer Care and Blood Disorders in the 21st Century, October 2019\n2.\tLoma Linda University School of Medicine – Grand Rounds, Advances in the Management of Sickle Cell Disease, March 2019.\n3.\tLoma Linda University School of Medicine – Experimental Therapeutics in Sickle Cell Disease – New Horizons at Loma Linda , November 2018 .\n4.\tAdventist Health Ukiah , California - Neurological Defects of Iron Deficiency and Lead Poisoning in Humans , October 2017\n5.\tHofstra NorthWell School of Medicine - National Public Health Symposium on Global Public Health , Convener and Moderator ,April 2016 \n6.\tCleveland Clinic Children’s Medical Center, Ohio – Non BCR-ABL Myeloproliferative syndromes of childhood, January 19, 2016.\n7.\tChildren’s Hospital at SMS Medical College ,India – Pediatric Hematology Oncology Emergencies for the Tropics, November 13, 2015 \n8.\tHarvard Medical School, Boston Children’s Hospital Division of Pediatric Hematology – Advances in Global Hematology, Annual Hemophilia Twining symposium, August 2, 2015.\n9.\tNew York Medical College as Grand Rounds, Division of Pediatrics – Emergencies in Pediatric Hematology and Oncology, April 2015.\n10.\tMaurice A. Deane School of Law, Hofstra University, New York - Healthcare Access to Undocumented immigrants: Immigration reform and its impact, March 2015.\n11.\tPediatric Academic Society/Society of Pediatric Research (PAS/SPR) as platform presentation, Vancouver, BC - Global Child Health in Rich & Poor Countries Lessons Learned from Indigenous Health, May 3 2014.\n12.\tDepartment of Medicine and Medical Oncology, as Guest International faculty , SMS Medical College, India - Advances in Stem Cell Transplantation – January 2014.\n13.\tInternational health conference, Global Association of physicians of Indian Origin , New Jersey – Impact of Lead Intoxication in Low to middle income countries , August 2012.\n14.\t139st APHA Annual Meeting and Exposition 2011, Boston - Use of decision support in a Harlem pediatric emergency department to increase prescription of controller medicines to patients with poorly controlled asthma - Wilson Wang, Carolina Valez, Nicole Falanga, Vikas Bhambhani , Akshat Jain , Farhad Gazi, David Spiller, Paper no-227188 , November 2011 \n15.\tThe New York Academy of Medicine, Resident award night - False negative result in newborn screening for Congenital Adrenal hyperplasia - July 2009.",institutionString:"Loma Linda University Children's Hospital",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Loma Linda University Children's Hospital",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"16",title:"Medicine",slug:"medicine"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"280415",firstName:"Josip",lastName:"Knapic",middleName:null,title:"Mr.",imageUrl:"https://mts.intechopen.com/storage/users/280415/images/8050_n.jpg",email:"josip@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. 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Vaccines usually contain drugs that resemble the microorganisms responsible for the disease and are often made from one of the killed or attenuated microorganisms, their toxins, or their surface proteins, introduced by mouth, by injection, or by nasal spray to stimulate the immune system in us and recognize the foreign agents and destroy them.
\nThere are many success stories in vaccine. The first vaccine, against smallpox, a disease that had killed millions of people over the centuries by British physician Edward Jenner in 1796 [1], was derived from the benign cowpox virus, which provided immunity to small pox. In 1980, following an historic global campaign of surveillance and vaccination, the World Health Assembly declared smallpox eradicated. In the nineteenth and twentieth centuries, scientists following Jenner’s model developed new vaccines to fight numerous deadly diseases, including polio, whooping cough, measles, tetanus, yellow fever, typhus, rubella mumps, varicella, and hepatitis B and many others [2]. Rabies was the first virus attenuated in a lab to create a vaccine for humans.
\nThe vaccine exposes humans to very small and safe amounts of attenuated or killed viruses and bacteria. When you are exposed to it in later life, the immune system will learn to recognize and attack infections. So you will not get sick, or you may be infected lightly. During the process of immunity development, the body produces antibodies against specific microorganisms and creates defense. The next time the person encounters that microorganism, the antibody prevents him from causing disease or alleviates the severity of the disease, regardless of the way that a vaccine is made.
\nVaccines are the most cost-effective healthcare interventions known to prevent death and disease. A dollar spent on a childhood vaccination not only helps save a life but greatly reduces spending on future healthcare. According to a new study from the University of North Carolina at Chapel Hill, vaccination efforts made in the world’s poorest countries since 2001 will have prevented 20 million deaths and saved $350 billion in healthcare costs by 2020 [3]. There are still numerous diseases causing globally significant morbidity and mortality, for which no vaccines are available. Millions of people worldwide die of malaria, tuberculosis, and AIDS every year, diseases without effective vaccines. This chapter describes the vaccine types now in use and that may lead to the vaccines of the future.
\nThere are several different types of vaccines. Each type is designed to boost your immune system and prevent serious, life-threatening diseases. Four types of vaccines are currently available:
live attenuated vaccines;
inactivated vaccines;
subunit, recombinant, polysaccharide, and conjugate vaccines; and
toxoid vaccines.
Live attenuated vaccines contain a version of the living virus that has been weakened so that it does not cause serious disease in people with healthy immune systems. Live attenuated vaccines can be made in several different ways. The most common methods involve passing the disease-causing virus through a series of cell cultures or animal embryos (typically chick embryos). Viruses are often attenuated by growing them in cells that they do not normally grow in for many generations. With each passage, the virus becomes better at replicating in new cells but loses its ability to replicate in human cells. Eventually, the attenuated virus will be less able to live in human cells and can be used in a vaccine. This method selects mutants that are more suitable for growth under abnormal culture conditions and is therefore less suitable for growth in natural hosts. Therefore, when attenuated viruses are given to a human, they are not able to replicate enough to cause illness like they would naturally but will still provoke an immune response that can protect against future infection. Albert Sabin’s oral polio vaccine and measles, rubella, mumps, and varicella vaccines are all achieved by in vitro cell culture passage selection clones. The poliovirus used in the Sabin vaccine is attenuated by the growth of monkey kidney epithelial cells. The measles vaccine contains a strain of rubella virus that grows in duck embryo cells and later grows in human cell lines [4, 5, 6, 7, 8]. Another live vaccine that has so far only been used in the military to prevent epidemic pneumonia includes adenoviruses 4 and 7 grown in human diploid cell lines and orally administered for replication in the intestine [9]. Other live vaccines that are attenuated in cell culture passages are attenuated monovalent rotavirus vaccines in Vero cells [10] and Japanese encephalitis virus strain SA14-14-2 [11]. Some viral vaccines are grown in chicken eggs; live attenuated influenza vaccine and yellow fever vaccines are currently produced in embryonated hen’s eggs, a method developed in the late 1930s [12, 13].
\nLive attenuated vaccines have advantages and disadvantages. Live attenuated vaccines are ideal for teaching the immune system against specific viruses because they are closest to natural infections. They often require only a single immunization, eliminating the need for repeated boosters. And these vaccines are relatively easy to create for certain viruses.
\nThe Sabine polio vaccine consists of three attenuated poliovirus strains that are orally administered to children in sugar cube or sugar liquid. The attenuated virus colonizes the gut and produces protective immunity against all three virulent poliovirus strains. Unlike most other attenuated vaccines that require a single immunization dose, the Sabin polio vaccine requires a booster because the three attenuated polioviruses in the vaccine interfere with each other’s replication in the gut.
\nThe main disadvantage of attenuated vaccines is the possibility they will revert to a virulent form and cause disease. These vaccines cannot be administered to people with weakened immune systems due to cancer, HIV, or other immune system depressing diseases. Attenuated vaccines also may be associated with complications similar to those seen in the natural disease. Live attenuated vaccines usually have to be refrigerated and protected from light. It can be difficult to ship these vaccines overseas and use them in places where there is lack of refrigeration. This technique does not work well for bacteria; therefore there are few live bacterial vaccines. The virus is very simple, but for bacteria, which have thousands of gene, is at least a hundred times larger than a typical virus. This makes bacteria more difficult to control and manipulate than viruses. Currently, scientists are trying to remove key genes from certain bacteria in order to create a weakened version for vaccines.
\nImmunization using this strategy are [14]:
\nViral:
MMR vaccine;
Rotavirus vaccine;
oral polio vaccine (not used in the USA);
influenza vaccine (nasal spray) FluMist;
varicella (chickenpox) vaccine;
shingles vaccine;
yellow fever vaccine;
adenovirus oral vaccine (military); and
Vaccinia vaccine.
Another common method of vaccine production is inactivation of the pathogen by heat or by chemical treatment. This destroys the pathogen’s ability to replicate but keeps it “intact” so that the immune system can still recognize it. Maintaining the epitope structure on the epitope antigen during inactivation is critical. Heat inactivation is generally unsatisfactory because it results in extensive denaturation of the protein; therefore, any epitope that is dependent on higher levels of protein structure may change significantly. Chemical inactivation with formaldehyde or formalin has been successful. The Salk polio vaccine is produced by formaldehyde inactivation.
\nBecause killed or inactivated pathogens cannot replicate at all, they cannot revert to a more virulent form capable of causing disease (as discussed above with live attenuated vaccines). Attenuated vaccines generally require only one dose to induce long-lasting immunity. However, inactivated vaccine tends to provide a shorter length of protection than live vaccines and is more likely to require boosters to create long-term immunity.
\nA vaccine consisting of orally administered killed cholera bacteria with or without the B subunit of cholera toxin has been developed [15]. Formalin-inactivated whole-cell pertussis vaccine was tested by Madsen [16], and later it was shown to be relatively successful in controlling severe disease [17]. In 1923, Glenny and Hopkins reduced the toxicity of diphtheria toxin by formalin treatment [18]. Ramon has improved this finding and has shown that it is possible to inactivate the toxicity of these molecules while retaining their ability to induce toxin-neutralizing antibodies [19]. In the twentieth century, chemical inactivation was also applied to viruses. Influenza vaccine was the first successful inactivated virus vaccine [20].
\nInactivated whole bio vaccines still present certain risks, even if they contain killed pathogens. When formaldehyde failed to kill all viruses in both vaccine batches, serious complications of the first Salk vaccines occurred, which led to a high proportion of polio (poliomyelitis).
\nInactivated vaccines are used to protect against:
hepatitis A;
flu (shot only);
polio (shot only); and
rabies.
The first vaccine, the smallpox vaccine, consists of live attenuated viruses, but it does not cause disease in human hosts. Many of the vaccines used today, including measles vaccines, yellow fever vaccine, and some influenza vaccines, use live attenuated viruses. Others use inactivated forms of toxins made from killed form of virus, debris of bacteria, or bacteria. The killed virus, bacterial debris, and inactivated toxins will not cause disease but will still cause immune reactions and prevent future infections. However, new techniques are also being developed to make different types of vaccines.
\nSubunit, recombinant, polysaccharide, and conjugate vaccines are biosynthetic vaccines. Biosynthetic vaccines contain man-made substances that are very similar to pieces of the virus or bacteria. The hepatitis B vaccine is an example.
\nSince these vaccines use only specific pieces of the germ, they show a very strong immune response, which targets the main part of the germ. It can also be used by almost everyone who needs them, including people with weakened immune system and long-term health problems. Vaccines consisting of specific purified molecules derived from pathogens can avoid some of the risks associated with attenuated or killed organism vaccines.
\nOne limitation of these vaccines is that you may need booster shots to get ongoing protection against diseases.
\nSubunit vaccines use only a subset of target pathogens to stimulate the immune system’s response. This can be done by isolating a specific protein from the pathogen and presenting it separately as an antigen. Acellular pertussis vaccines and influenza vaccines (injected forms) are examples of subunit vaccines.
\nAnother subunit vaccine can be created by genetic engineering. The gene encoding the vaccine protein is inserted into another virus or inserted into a cultured production cell. Vaccine proteins are also produced when the vector virus is propagated. The result of this approach is a recombinant vaccine: the immune system will recognize the expressed protein and provide future protection against the target virus. Many genes encoding surface antigens from viral, bacterial, and protozoal pathogens have been successfully cloned into bacterial, yeast, insect, or mammalian expression systems, and the expressed antigens are used for vaccine development. A hepatitis B vaccine that is approved for use in humans is a recombinant vaccine. The vaccine was developed by cloning the hepatitis B virus surface antigen (HBsAg) gene and expressing it in yeast cells. Recombinant yeast cells proliferate in large fermenters, and HBsAg accumulates in cells. At the end of the fermentation, recombinant HBsAg are harvested by disrupting yeast cells, which is then purified by biochemical techniques. This recombinant hepatitis B vaccine has been shown to induce the production of protective antibodies [21, 22].
\nHuman papillomavirus (HPV) vaccine is another vaccine made using genetic engineering. Two types of HPV vaccine are available, Gardasil (marketed by Merck and protecting against types 6, 11, 16, and 18 of the human papillomavirus) and Cervarix (marketed by GlaxoSmithKline and protecting against types 16 and 18 only). Both are made in the same way: for each strain, a single viral protein was isolated. When these proteins are expressed, viruslike particles (VLPs) are produced. These VLPs contain no genetic material that causes disease but promote immune responses and protect future HPV infection.
\nRecombinant vector vaccines use attenuated viruses (or bacterial strains) as vectors. A gene encoding a major antigen of a particularly virulent pathogen can be introduced into an attenuated virus or bacterium. The attenuated organism acts as a vector that replicates and expresses the gene product of the pathogen in the host.
\nBaculovirus which is a virus that infects only insects can be used as a vector, and genes for specific immunogenic surface proteins of influenza virus can be inserted. Once the modified virus is introduced into humans, the immunogen is expressed and displayed, producing an immune response against the immunogen and producing an immune response to the immunogen from which it is derived. In addition to insect viruses, human adenoviruses have been identified as potential carriers for recombinant vaccines, particularly against diseases such as AIDS. Vaccinia virus, the attenuated vaccine used to eradicate smallpox, was the first used in live recombinant vaccine approaches [23]. This large, complex virus, with a genome of about 200 genes, can be designed to carry dozens of foreign genes without compromising their ability to infect host cells and replicate. Experimental recombinant vaccinia strains have been designed to provide protection against influenza, rabies, and hepatitis B and other diseases.
\nDNA vaccines consist of plasmid DNA encoding antigenic proteins which are injected directly into the muscle of the recipient. The DNA itself inserts into the individual’s cells, which then produce the antigen from the infectious agent. DNA vaccines have advantages over many existing vaccines. For example, the encoded protein is a native form of the host and has no denaturation or alteration. Therefore, the immune response is identical to the antigen expressed by the pathogen. The handling and storage of plasmid DNA do not require refrigeration, a feature that greatly reduces the cost and complexity of delivery. At present, there are human trials underway with several different DNA vaccines, including those for malaria, AIDS, influenza, and herpesvirus. Researchers hope that DNA vaccines can produce immunity against parasitic diseases such as malaria; however, there is currently no human vaccine in use for fighting parasites [24].
\nConjugate vaccines are somewhat similar to recombinant vaccines: they are prepared using a combination of two different components. The conjugate vaccine was prepared using fragments from the coats of bacteria. These coatings are chemically linked to a carrier protein which is used as a vaccine. Conjugate vaccines are used to produce a more powerful co-immune response: in general, the presented “fragments” of the bacteria do not themselves produce a strong immune response, while the carrier protein produces a strong immune response. This fragment of bacterium does not cause disease, but when combined with carrier proteins, it can produce immunity against future infections. The vaccines currently in use for children against pneumococcal bacterial infections are made using this technique.
\nThese vaccines are used to protect against:
Haemophilus influenzae type b (Hib) disease;
hepatitis B;
human papillomavirus (HPV);
whooping cough (part of the DTaP combined vaccine);
pneumococcal disease;
meningococcal disease; and
shingles.
Toxoid vaccines are made from selected toxins that have been sufficiently attenuated and are able to induce a humoral immune response. These toxins produce many of the symptoms of the disease. For example, diphtheria and tetanus vaccines can be prepared by purifying bacterial toxins and then inactivating toxin with formaldehyde to form a toxoid. Inoculating with a toxoid induces an anti-toxoid antibody that is also capable of binding toxins and neutralizing their effects.
\nToxoid vaccines tend not to have a duration of immunity comparable to attenuated viral vaccines; therefore, toxid vaccines, like some other types of vaccines, may need booster shots to get ongoing protection against diseases. Revaccination (booster) may be required multiple times in a single year depending on individual patient risk factors.
\nToxoid vaccines are used to protect against:
diphtheria; and
tetanus.
There are still the needs for vaccines against other diseases. Millions of people worldwide die of malaria, tuberculosis, and AIDS every year, among which there are no effective disease vaccine. The road to successful development of vaccines that can be approved for human use, reasonably manufactured cost, and effective delivery to high-risk groups is expensive, long, and tedious.
\nResearchers continue to develop new vaccine types and improve current approaches.
\nThis work was supported by the National Natural Scientific Foundation of China (Grant Nos. 81673117 and 81573140).
\nWe have no conflict of interest.
The north-eastern state of Assam is known for its rich biodiversity and considered as biological hotspot with many rare and endemic plant and animal species. Out of total 78,438 sq. km geographical area of the state, the forest area covers around 24.58% area. The moderate dense forests areas which are mainly extended through districts of Karbi Anglong, NC Hills, Cachar, Karimganj, Hailakandi, northern part of Kokrajhar, Bongaigaon and southern part of Kamrup, Tinsukia, are vulnerable to frequent flood incidents. The Brahmaputra River and its tributaries, flowing from north-east to south-west, are the mainly responsible for the periodic floods in Assam State. Along with flood events, the incidence of forest fires in the deciduous forests during summer season, i.e. March to April, causing a wide spread disturbance in the forest eco-system. Assam State has 5 National Parks and 16 Wildlife Sanctuaries under protected area (PA) network and constituting 4.98% of the geographical area. The protected areas can act as benchmark for differentiating the ecological disturbance from the natural fluctuation [1]. Hence, regular monitoring of PA’s is crucial for detecting the rapid changes in functional attributes as well as to identify areas that need to adapt or modify to meet the challenges posed by global warming [2].
\nThe understanding of the global carbon cycle is being affected due to the existing spatio-temporal variability of eco-system disturbance and resultant emissions from loss of terrestrial biomass [3, 4, 5, 6, 7, 8]. Hence, the regular monitoring and assessment of the ecological disturbance is essential for understanding the cause and effect of the disturbances and subsequent effective management of the forest ecosystems. With the advent of multispectral and thermal remote sensing technology, the earth observation satellites data became more effective for monitoring biodiversity. The altered ecosystem structure and functions due to sustained disturbance in Woody ecosystem can be captured by remote sensing for mapping the extent and location of the disturbance [9, 10]. The effectiveness of the management practices or impact of global environment changes in the forest areas, especially Protected Area (PA), can be successfully carried out using satellite remote sensing [11, 12]. The technology can also provide valuable information on the alteration of landuse, productivity or phenology [13].
\nThe MODIS global disturbance index (MGDI) was first proposed and used by [14] for assessing the disturbance in woody ecosystems of North America. The MGDI was conceptualized based on the fact that the surface temperature decreases with the increase in vegetation density through the latent heat transfer [15, 16]. The index was further utilized for assessing the impact of cyclones on the ecological disturbance of mangrove forest of Sundarbans. For further details about the concept and computation of MGDI, one can refer [14] or [16].
\nIn the present study, MODIS global disturbance index (MGDI) was used to assess the ecological disturbance caused by two different kinds of natural hazards, viz. river flood and forest fire, in the perennial forest ecosystem of Assam State during 2001 to 2011. The flood and forest fire induced disturbed areas were identified based on the MGDI based thresholds and the spatio-temporal dynamics of the disturbance over the Assam forest area was studied. Finally, a classified geo-spatial product of disturbed prone forests was generated based on estimated disturbed area during the entire study period.
\nAssam State, situated at the north-east of India and foothills of the eastern Himalayas, covers an area of 78,438 sq. km and lies in the middle reach of the Brahmaputra River and Barak (
(a) Location of the study area in India (b) flood and fire prone forests.
In the present study, the ecological disturbance regime of the Assam forest area, India has been analyzed. Based on the intensity of flood and fire incidence, total 16 forests have been selected for MGDI based thresholds development and discrimination of the disturbed areas. The details of the selected forests, i.e. eight for each of flood and forest fire, were shown in Figure 1. The flood prone forests were mainly situated along the Brahmaputra River, whereas the fire prone forests were distributed throughout the Assam State.
\nThe 16-day composite Enhanced Vegetation Index (EVI) data products (MOD13Q1) and 8-day composite Land Surface Temperature (LST) data products (MOD11A2) for the period of 2001 to 2011 were downloaded from the MODIS web-site (
The forest boundaries of Assam State were generated by digitizing the Survey of India Topomaps at 1:50,000 scale. According to the World Database on Protected Areas (
The date wise flood maps were downloaded from National Remote Sensing Centre (NRSC) web site (
Flood intensity map of Assam State (www.nrsc.gov.in).
Date wise forest fire information for Assam State was collected from MODIS site (
Forest fire intensity map.
Year | \nRifu | \nManas | \nSonai Rupai | \nKaliyani | \nLangting Mupa | \nNorth Cachar | \nBarail | \nBadsahitila | \n
---|---|---|---|---|---|---|---|---|
2001 | \n15 | \n1 | \n10 | \n0 | \n1 | \n1 | \n2 | \n18 | \n
2002 | \n2 | \n23 | \n1 | \n1 | \n2 | \n0 | \n1 | \n16 | \n
2003 | \n4 | \n18 | \n18 | \n4 | \n20 | \n19 | \n40 | \n219 | \n
2004 | \n12 | \n17 | \n55 | \n5 | \n44 | \n20 | \n26 | \n96 | \n
2005 | \n12 | \n6 | \n18 | \n6 | \n64 | \n11 | \n25 | \n86 | \n
2006 | \n35 | \n13 | \n32 | \n6 | \n41 | \n31 | \n58 | \n158 | \n
2007 | \n6 | \n6 | \n19 | \n12 | \n43 | \n17 | \n45 | \n252 | \n
2008 | \n4 | \n4 | \n41 | \n16 | \n25 | \n7 | \n27 | \n108 | \n
2009 | \n52 | \n24 | \n54 | \n18 | \n71 | \n33 | \n84 | \n157 | \n
2010 | \n11 | \n17 | \n21 | \n4 | \n165 | \n11 | \n41 | \n212 | \n
2011 | \n36 | \n23 | \n29 | \n2 | \n64 | \n16 | \n14 | \n91 | \n
Forest fire events for selected Assam State forests (2001–2011).
The MODIS global disturbance index (MGDI) was developed based on the concept that any perceptible disturbance of ecology will result in a significant alteration in vegetation and a concomitant change in the land surface temperature [14, 16].
\nIn the present study, the flood and forest fire were selected as the causative factors that create ecological disturbance to address both the non-instantaneous and instantaneous disturbance, respectively. In case of instantaneous disturbance like forest fire, the disturbance is manifested immediately after the event, resulting in immediate increase in LST with decreased vegetation cover. On the contrary, non-instantaneous disturbance like flood will not trigger immediate change in either LST or EVI due to availability of abundant moisture for evaporation to offset the loss of transpiration. Whereas, in the following year the effect of flood damage was evident due to vegetation mortality and severe structural damage, which will eventually lead to increase in annual maximum LST due to the reduction in transpiration [14].
\nThe instantaneous (MGDIinst\n) and non-instantaneous (MGDInon-inst\n) MGDI were computed using the following equations:
\nWhere, MGDIinst\n and MGDInon-inst\n are the instantaneous and non-instantaneous MGDI value, respectively. LSTmax\n and EVImax\n are the annual maximum 16-day composite LST (°C) and EVI, respectively. EVImax-post\n is the maximum 16-day composite EVI following the LST\nmax\n, current year (y) is the year being evaluated for disturbance and multi-year mean (y − 1) is the mean of the ratios excluding the current year [14, 16].
\nA two-step methodology, as explained by Dutta et al. [16], was adopted for to discriminate the disturbed forest areas caused due to flood and forest fire. In the 1st step, the % change in MGDI values were calculated based on the time-series data for each pixel. Whereas in the second step the MGDI based thresholds were estimated for flood and forest fire, separately. The Percentage change in MGDI for both the instantaneous and non-instantaneous disturbance were calculated using the following equation:
\nAs discussed earlier, the forests prone to flood and fire were selected based on the temporal occurrence of the natural disturbance. Total 16 representative forests frequently affected by flood and forest fire were extensively analyzed to develop the thresholds for flood and forest fire separately based upon the % change of MGDI over multi-year mean. The spatio-temporal variation of the % change in MGDInon-inst\nover the Assam forest area was shown in Figure 4 for some selected years.
\nPercent change in MGDInon-inst over the Assam forest area.
The year-wise % change in MGDI was generated for all the representative forests wherein only the flood affected pixels were considered. Similarly, year-wise % change in MGDI was generated for the pixels undergone forest fire. The temporal profile of the percent change in MGDI of each forest was compared with the area weighted flood and fire intensity, to confirm the effect of natural disturbances on the MGDI. The multi-year mean value plus one standard deviation of the % change in MGDI was considered to be the threshold, and the value was used for discrimination of the disturbed pixels [16]. Due to the slow and gradual impact of flood, unlike forest fire, a lower disturbance threshold was estimated in case of flood. The % change of MGDI greater than 7% and 11% of the temporal mean was fixed for discriminating the non-instantaneous (flood) and instantaneous (forest fire) disturbed pixels.
\nThe selected thresholds were applied on the % change MGDI images (both non-instantaneous and instantaneous, separately) for identifying the year-wise disturbed forest areas. The year-wise % disturbed area was estimated for each forest and the temporal profiles were used to analyze the disturbance intensity at spatio-temporal scale. Upon integration of the year-wise disturbed area, disturbance prone maps were generated for both instantaneous and non-instantaneous events.
\nThe summary statistics of the flood affected forests is shown in Table 2. According to the % disturbed area it was found that the year 2003, 2008, 2009 and 2010 were the most disturbed years caused by river flood in comparison to rest of the years. These findings are in corroboration with the rainfall data collected from Indian Meteorological Department (
Year | \nPhathasil | \nBuraMayang | \nPobitora | \nOrang | \nKamakhya Hills | \nKukrakata Hills | \nKaziranga | \nDihing mukh | \n
---|---|---|---|---|---|---|---|---|
2001 | \n8.4 | \n1.2 | \n4.7 | \n8.4 | \n6.7 | \n2.0 | \n1.4 | \n1.4 | \n
2002 | \n7.4 | \n9.1 | \n8.4 | \n4.3 | \n7.9 | \n2.0 | \n3.4 | \n4.3 | \n
2003 | \n39.1 | \n31.2 | \n17.1 | \n10.4 | \n29.6 | \n9.3 | \n4.0 | \n6.1 | \n
2004 | \n7.2 | \n5.4 | \n4.0 | \n3.0 | \n7.5 | \n4.1 | \n0.7 | \n1.4 | \n
2005 | \n0.5 | \n1.1 | \n0.0 | \n2.6 | \n0.0 | \n0.0 | \n0.3 | \n3.3 | \n
2006 | \n0.4 | \n1.5 | \n0.9 | \n3.6 | \n2.5 | \n0.0 | \n0.1 | \n2.9 | \n
2007 | \n4.8 | \n8.5 | \n14.0 | \n4.1 | \n8.8 | \n1.1 | \n2.8 | \n5.8 | \n
2008 | \n18.9 | \n9.0 | \n2.5 | \n10.0 | \n12.9 | \n17.8 | \n0.9 | \n7.4 | \n
2009 | \n28.0 | \n10.2 | \n10.2 | \n12.4 | \n2.5 | \n6.1 | \n2.6 | \n9.4 | \n
2010 | \n12.2 | \n24.0 | \n30.1 | \n8.1 | \n34.6 | \n22.8 | \n14.2 | \n20.6 | \n
2011 | \n1.9 | \n1.2 | \n0.6 | \n11.8 | \n2.5 | \n11.1 | \n2.0 | \n2.1 | \n
Percent disturbed area caused by flood in selected Assam State forests.
The disturbed area maps of the Assam forests showed (Figure 5) that the area under disturbance was much higher in the year of 2003, 2008 and 2010 in comparison to others, whereas it was minimum in the year of 2006. The flood intensity maps (Figure 2) showed that the extent of flooded area is mainly confined around the Brahmaputra and Barak River valley, but it was interesting to note that a subset of the flood pixels were marked as disturbed pixels (Figure 5). Hence, the temporal frequency of flood along with extent was a decisive factor whether a pixel was disturbed or not. For example, in BuraMayang around 80% of the total forest area was under flood during 2008 with frequency value of one, whereas during 2010 around 40% forest area was inundated by flood with frequency more than 10. Consequently, the disturbance was recorded in 9% of the total forest area in 2008, whereas it was around 24% during 2010. Similarly, in case of Pobitora the whole forest was under flood during both 2008 and 2010, but due to the difference in flood frequency the disturbed area were 2.5 and 30.1% of the total area, respectively.
\nThe disturbed area maps of Assam forests shows higher disturbances in the 2003, 2008 and 2010 and a minimum in 2006.
The temporal dynamics of disturbed area, caused by river flood, for two selected forests, namely Kamakhya and Kukrakata Hills was shown in Figure 6. In case of Kamakhya Hills the year 2010 was found to the most disturbed year, followed by 2003 and 2008. Hardly any disturbance was noticed during 2005, 2006, 2009 and 2011. Similarly, in case of Kukrakata Hills also three major flood events were observed in 2010, 2008 and 2003. Though the major flood years were common in both the cases, their magnitude varies.
\nTemporal dynamics of disturbed area caused by river flood for two selected forests of Assam state.
The distribution of disturbed area caused by forest fire is shown in Table 3. Unlike flood, the spatial extent of % disturbed area caused by forest fire was much lower as the fire is a localized phenomenon. A maximum value of 3.5% of the total forest area was disturbed due to the fire during 2010 in Barail forest. More than 2% of the forest area was affected in Sonai Rupai, Langting Mupa, Barail and Badsahitila forests during 2003. Whereas in 2010 more than 1% of the total forest area of Sonai Rupai, North Cachar and Barail was affected.
\nYear | \nRifu | \nManas | \nSonai Rupai | \nKaliyani | \nLangting Mupa | \nNorth Cachar | \nBarail | \nBadsahitila | \n
---|---|---|---|---|---|---|---|---|
2001 | \n0.18 | \n0.00 | \n0.05 | \n0.00 | \n0.01 | \n0.01 | \n0.00 | \n0.14 | \n
2002 | \n0.00 | \n0.00 | \n0.03 | \n0.26 | \n0.18 | \n0.00 | \n0.00 | \n0.12 | \n
2003 | \n0.28 | \n0.26 | \n2.11 | \n0.53 | \n1.80 | \n0.98 | \n1.88 | \n3.73 | \n
2004 | \n0.24 | \n0.23 | \n0.07 | \n0.13 | \n0.98 | \n0.08 | \n0.07 | \n0.73 | \n
2005 | \n0.01 | \n0.01 | \n0.67 | \n0.13 | \n0.15 | \n0.16 | \n0.60 | \n0.34 | \n
2006 | \n0.01 | \n0.01 | \n0.00 | \n0.00 | \n0.20 | \n0.11 | \n0.16 | \n0.00 | \n
2007 | \n0.00 | \n0.00 | \n0.23 | \n0.39 | \n0.29 | \n0.25 | \n0.48 | \n0.28 | \n
2008 | \n0.07 | \n0.08 | \n1.78 | \n0.34 | \n0.26 | \n0.31 | \n0.58 | \n0.05 | \n
2009 | \n0.34 | \n0.46 | \n0.46 | \n0.00 | \n0.28 | \n0.31 | \n0.23 | \n1.39 | \n
2010 | \n0.84 | \n0.44 | \n1.55 | \n0.05 | \n0.00 | \n1.34 | \n3.44 | \n0.69 | \n
2011 | \n0.45 | \n0.17 | \n0.23 | \n0.06 | \n0.06 | \n0.12 | \n0.44 | \n0.11 | \n
Year-wise percentage disturbed forest area caused by forest fire for selected forests of Assam State.
It was noteworthy that unlike flood, forest fire intensity was not in direct corroboration with disturbed area statistics (Tables 1 and 3). As discussed earlier, the point locations of forest fire were converted to fire intensity information using 1 km grid, to make it spatially contiguous, as the extent of forest fire information was not available. Hence, the discrepancy between the disturbed area statistics and fire frequency may be attributed to lack of spatial representation of fire extent. In addition frequent fire incidences might have hindered the process of re-generation and vegetative growth of the forest causing insignificant changes in the MGDI values in post incidence dates. For example, in case of Rifu forest the fire frequency was 52 and 36 during 2009 and 2011, respectively, but the disturbed area was 0.34 and 0.45% of the total forest area. On the other hand, 0.84% of the forest area was found to be disturbed during 2010 with only 11 fire incidences. Similar kind of observation was found in case of Badsahitila also, where the fire frequency was more than 150 times during 2003, 2006, 2007, 2008, 2009 and 2010, but the % disturbed area were 3.73, 0.21, 0.28, 0.05, 1.39 and 0.69, respectively.
\nThe temporal dynamics of disturbed area induced by the forest fire for two selected forests, namely Badsahitila and Sonai Rupai, were shown in Figure 7. In case of Badsahitila, the major disturbance due to forest fire was found during 2003, followed by the year 2009, whereas during 2001, 2002, 2005, 2006, 2007, 2008 and 2011 very less area was noted to be disturbed due to the fire incidences. On the other hand, in case of Sonai Rupai three major disturbances were noted during 2003, 2008 and 2010, with two other intermediate disturbances during 2005 and 2009. The major fire incidents were reported from moist deciduous forest and grass lands.
\nTemporal dynamics of disturbed area caused by the forest fire for selected forests of Assam state.
The spatial distribution of both the non-instantaneous and instantaneous forest disturbances maps have been generated and presented in Figures 8 and 9 respectively. In non-instantaneous disturbance the effect is not triggered immediately in terms of changes in LST and/or EVI. In contrast post-event effect is immediately exhibited due to changes in LST and EVI, for example, in case of forest fire both the LST increases and the EVI changes drastically. Based upon the percent change of MGDI, both the disturbance types are classified into low, medium and high category to spatially depict the disturbance regime. It was seen that most of the non-instantaneous disturbed area falling under “low” category, followed by “moderate”. Patches of “highly disturbed” areas are observed in north of Tinsukia district which falls under the flood plain of Brahmaputra River. Scattered patches of “highly disturbed” areas also noticed along the northern boundary of the Assam state adjoining to Bhutan, Kokrajhar and at the border of Karbi Anglong (East) and Golaghat districts. Under instantaneous disturbance regime most of the forest areas are falling under “low” disturbance category presumably due to high threshold value. Notably the forests of north Tinsukia district falls under “highly disturbed” category in both the instantaneous and non-instantaneous disturbance.
\nSpatial distribution of non-instantaneous disturbance categories.
Spatial distribution of instantaneous disturbance categories.
The ecological disturbance regime of the Assam forest area was assessed using Global Disturbance Index derived from the time-series MODIS EVI and LST data. The % change in MGDI from its multi-year mean was found to be in good agreement with the flood as well as forest fire intensity. The thresholds for non-instantaneous disturbance, i.e. flood, was found to be lower than the instantaneous disturbance, i.e. forest fire. The time-series disturbed area maps were able to capture the spatio-temporal dynamics of the disturbance regimes. The high disturbed area due to flood were in good agreement with the high rainfall year. The temporal profiles of the forest specific disturbed area could able to distinguish the major disturbed years. The disturbed prone area maps were able to classify the Assam forest areas into three major classes, which can be further utilized for the better management of the forest areas. The main assumption of the study was that the disturbances were created due to two natural hazards, like flood and forest. However, disturbances can be caused by disease/pests, anthropogenic interference, climate change etc. which needs to be examined. Hence, future study can be adopted for estimating the disturbance regime using multiple factors with an intensive ground data support. In the present study, forest fire events was used for estimating the fire intensity, whereas with the aid of the forest fire extent the present methodology would have been more robust. Sensors with better spatial resolution would increase the estimation accuracy of the disturbed area for localized disturbance.
\nThe authors are thankful to the Director, NRSC and Chief General Manager (Regional Centres), for their continuous support and encouragements during the investigation. We duly acknowledge the MODIS data site for time-series data supply and forest fire information. We also acknowledge the Disaster Management Support Service Group, NRSC, for providing the flood inundation maps.
\nThe authors declare no conflict of interest.
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