Run time results for the simplified M50 occupant model.
\r\n\tAs the subject of adhesives is in constant development, this book's purpose is to get together information about adhesives science and technology, recent advances, and applications that use adhesive technology. Also, to make these contents available to engineering students, engineers, researchers, and the people interested in this topic. The book is expected to present works that aim to contribute to the development of new technologies and the use of non-traditional materials in engineering.
",isbn:"978-1-83880-670-5",printIsbn:"978-1-83880-669-9",pdfIsbn:"978-1-83880-671-2",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,isSalesforceBook:!1,isNomenclature:!1,hash:"c58b7d4c17e2a202af1dc4b906b7becb",bookSignature:"Prof. António Bastos Pereira and Dr. Alexandre Luiz Pereira",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/11819.jpg",keywords:"The Technology of the Adhesives, Recent Advances, New Perspectives, Structural Adhesives Bonding, Durability of Structural Adhesives, New Applications, Repair of Composites, Bonding of Composites, Experimental Mechanics Tests, Thermal Analysis, Finite Element Method, Numerical Analysis.",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 15th 2022",dateEndSecondStepPublish:"June 22nd 2022",dateEndThirdStepPublish:"August 21st 2022",dateEndFourthStepPublish:"November 9th 2022",dateEndFifthStepPublish:"January 8th 2023",dateConfirmationOfParticipation:null,remainingDaysToSecondStep:"15 days",secondStepPassed:!0,areRegistrationsClosed:!1,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. António Pereira is a professor and researcher, who graduated from the University of Porto, and gained experience as an engineer working at Renault, with an h-index of 23, and more than 1500 citations for 70 papers published in SCI journals.",coeditorOneBiosketch:"An active researcher in Solid Mechanics, Dr. Alexandre Luiz Pereira holds a degree in Mathematics from the State University of Rio de Janeiro, and a degree in Mechanical Engineering from the Fluminense Federal University in Brazil.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"211131",title:"Prof.",name:"António",middleName:"Bastos",surname:"Pereira",slug:"antonio-pereira",fullName:"António Pereira",profilePictureURL:"https://mts.intechopen.com/storage/users/211131/images/system/211131.png",biography:"Founding shareholder and Director of Martifer Group (ca. 3500 employees) (1990-1999) - was responsible for the planning and production of about 500 steel structures and industrial equipment with a total amount exceeding 100 million euros.\nAssistant Professor at the Department of Mechanical Engineering, University of Aveiro, since 2000. Board Member and Member of the Executive Committee at the Department of Mechanical Engineering, University of Aveiro (2011 – 2015), currently Director of TEMA - Centre for Mechanical Technology and Automation.\nHis main research area has been mechanics of composite materials, with particular emphasis on delamination fracture mechanics. He has published 44 papers in SCI journals and has delivered 30 presentations at international conferences. 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Churchill, Maja Dutour Sikirić, Božana Čolović and Helga Füredi Milhofer",coverURL:"https://cdn.intechopen.com/books/images_new/8812.jpg",editedByType:"Edited by",editors:[{id:"219335",title:"Dr.",name:"David",surname:"Churchill",slug:"david-churchill",fullName:"David Churchill"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"56773",title:"Iron Deficiency Anemia in Children",doi:"10.5772/intechopen.69774",slug:"iron-deficiency-anemia-in-children",body:'Iron deficiency is the most common micronutrient deficiency worldwide and one of the most important public health problems, affecting approximately 25% of the world’s population according to the World Health Organization (WHO). Iron deficiency is the most common in preschool children and women of childbearing age, particularly in regions of Asia and Africa with poor access to iron-rich foods [1, 2]. There are lower rates of iron deficiency in developed countries such as the United States and other industrialized regions with healthy food rich in nutrients. However, the problem still exists and can have a great impact on mental and physical development, health maintenance, and the quality of life of affected children.
Approximately 8% of toddlers in the United States have iron deficiency, and 2–3% have iron deficiency anemia (IDA) [3]. As age increases, prevalence decreases until adolescence. Sixteen percent of adolescent girls have iron deficiency, and 3% have IDA [4]. Among American females aged 12–15 years, the incidence of iron deficiency was 9% and the incidence of IDA was 2%; in the age group 16–19 years, the incidence was 11 and 3%, respectively [5]. Less than 1% of adolescent males had iron deficiency. Higher incidence of iron deficiency was found in both male and female adolescents in some other countries [6, 7]. The rate of iron deficiency did not decline much during the last 40 years, but there were significant improvements in some subgroups of young children. For example, in children aged 12–24 months, iron deficiency rates declined from 23 to 11% between two study periods [3].
The prevalence of iron deficiency in the United States is higher in children who live in poverty, in low-income families, and in immigrant groups. The highest prevalence was shown in children with African-American and Hispanic origin [3, 8]. Other risk factors associated with higher prevalence of IDA are low birth weight, prematurity, and childhood obesity [3, 8, 9]. These high-risk pediatric subgroups should undergo screening.
Pinhas-Hamiel and co-workers showed that the prevalence of iron deficiency was significantly associated with increased body mass index (BMI) [10]. Obesity was a risk factor in both males and females, but it was about three times higher in girls [10, 11]. It is unclear why obesity is linked to iron deficiency and IDA, but low-quality foods and increased needs comparing to body weight may be connected.
Adolescent athletes, vegetarians, adolescents with chronic illnesses, heavy menstrual blood loss (>80 ml/month), or children who are underweighted or malnourished are at higher risk for iron deficiency and IDA, and they should also have laboratory screening for anemia [12, 13].
In developing countries, where diets do not contain sufficient red meat, IDA is approximately seven times more frequent than in Europe or North America. Despite the fact that there is enough dietary iron in some cases, this is the case because heme iron is absorbed better than nonheme iron. IDA was found in 2/3 of children and adolescents in Nepal and in Sudan [14], and in 48.5% of Egyptian children in 2005 [15]. Parasites like hookworm can worsen iron deficiency due to profound gastrointestinal blood loss.
Neonates have total body iron of 250 mg (80 mg/kg), obtained from maternal sources. In the first 6 months of life, during the period when the infant gets iron-deficient milk diet, this amount decreases to 60 mg/kg. Infants fed with cow’s milk are at greater risk to develop serious IDA because calcium from cow’s milk is competing with iron for absorption. Children should get 0.5 mg more iron than is lost daily in order to maintain a normal body iron of 60 mg/kg.
The prevalence of iron deficiency exceeds 50% in countries with limited food and nutrient sources, such as most countries in Africa, Southeast Asia, and Latin America [16]. The prevalence of anemia ranges from 45 to 65% in children, 20 to 60% in women, and 10 to 35% in men [1]. Half of these cases are presumed to be caused by iron deficiency.
The prevalence of IDA is still high in infancy and preschool children, despite improvements in public health awareness, increased breastfeeding rate, and the presence of iron-fortified foods in diet [17, 18]. All these facts emphasize the importance of constant surveillance and early detection, prevention, and intervention toward iron deficiency in childhood, particularly in high-risk groups. Special attention should be paid to discover and treat iron deficiency during pregnancy and the earliest periods of life, because severe iron deficiency can have a great impact on child’s growth, development, and learning skills.
Iron deficiency is a condition when the body lacks sufficient iron to maintain normal physiological functions. It is defined as decreased total body iron or, in some cases, by serum ferritin level <12 mg/l in children up to 5 years and <15 mg/l in children 5 years and older. Although the serum ferritin level is useful in defining iron deficiency, this definition can be considered only if other conditions that can affect ferritin levels (i.e., inflammation or liver disease) are absent. For children less than 5 years of age with concurrent infection, serum ferritin concentrations <30 mg/l are reflective of depleted iron stores [19].
Anemia is defined as a hemoglobin concentration more than 2 standard deviations below the mean reference value for age- and sex-matched healthy population. WHO hemoglobin thresholds used to define anemia in different age groups are [2]:
children 6 months to 5 years: 11 g/dl;
children 5–12 years: 11.5 g/dl;
children 12–15 years: 12 g/dl;
nonpregnant women: 12 g/dl;
pregnant women: 11 g/dl; and
men ≥15 years: 13 g/dl.
IDA develops when body iron is too low to maintain normal red blood cell (RBC) production. IDA in young children (up to 5 years) is defined as the presence of ferritin level <12 mg/l and hemoglobin level <11 g/dl, in the absence of other conditions that can affect these findings [20].
The terms “iron deficiency” and “IDA” are often used in the same context. However, iron deficiency without anemia is three times as common as IDA. If iron requirements are below iron intake, total body iron reduces gradually. Hemoglobin levels are initially normal, reflecting the stage when iron deficiency exists in the absence of anemia. At that point, ferritin level and transferrin saturation are reduced. As total body iron decreases and iron stores are exhausted, hemoglobin levels drop below normal values. Thus, iron deficiency is defined as reduced body iron but hemoglobin levels are still above the cut-off value for anemia. Worsening of that condition leads to iron-deficient erythropoiesis and finally to development of IDA.
Iron is an essential micronutrient in the human body. It plays an important role in many metabolic processes, such as oxygen transport, electron transport, and DNA synthesis. Iron is a component of many cellular proteins and enzymes. Heme proteins, hemoglobin and myoglobin, contain about 3/4 of total body iron. The rest of body iron is stored in ferritin and hemosiderin, and about 3% is part of enzyme systems, such as catalase and cytochromes [21]. Iron is mostly recycled from senescent RBCs by macrophages. Only a small proportion of total body iron enters and leaves the body on a daily basis. Consequently, mechanisms that affect intestinal absorption and intercellular iron transport have great impact on iron balance. The serum iron concentration is regulated by absorptive cells in the proximal small intestine, which can regulate iron absorption to compensate for iron body loss. There are three different pathways of iron uptake in the small intestine: the heme pathway and two specific pathways for ferric and ferrous iron, respectively.
Enterocytes absorb heme iron and nonheme iron noncompetitively. Dietary iron contains both chemical forms of iron. Heme iron is mainly found as ferrous iron (Fe2+), while the most part of nonheme dietary iron is ferric iron (Fe3+). When heme enters the enterocyte, it is degraded by heme oxygenase with release of iron. It passes the basolateral membrane of the enterocyte and competes with nonheme iron to bind transferrin in the plasma. The way of nonheme iron transport in the body is still not known. The concentration of iron in the enterocytes depends on the body’s needs for iron. Individuals who are iron-deficient have a small amount of iron in enterocytes, while those who have sufficient body iron have higher amounts of iron in the absorptive intestinal cells. Iron in the enterocyte regulates absorption by either up-regulation of receptors or saturation of an iron-binding protein, or both. Iron that is delivered to other nonintestinal cells in the body is bound to transferrin. There are two pathways through which transferrin iron can be delivered into nonintestinal cells: classical transferrin receptor pathway and the pathway independent of the transferrin receptor.
In adults, only 5% of total body iron requirements is from different food sources. This amount is the same as iron loss, which is mainly from the gastrointestinal tract. The majority (95%) of iron comes from the breakdown of old RBCs. In children, approximately 30% of iron comes from diet, probably due to fast growth in pediatric age [21, 22].
There are three major factors that can influence intestinal iron absorption: iron stores in ferritin and transferrin, erythropoietic rate, and bioavailability of iron in foods. When iron stores decrease, receptors in the intestinal mucosa increase in order to raise iron uptake. Iron absorption also increases when there is increased or ineffective erythropoiesis.
During the intrauterine period, the only source of iron is the iron that is crossing through the placenta. The majority of healthy infants have iron stores of about 80 mg/kg, and 2/3 of total iron is bound in hemoglobin molecules. Normal hemoglobin concentration is 15–17 g/dl. Healthy infants have enough body iron for the first 5–6 months of life [22, 23]. There are some conditions that can reduce iron stores at birth or can act through other mechanisms, thus increasing the risk for developing IDA during the first months of life. These conditions are maternal iron deficiency, prematurity, administration of erythropoietin for anemia of prematurity, fetal-maternal hemorrhage, twin-twin transfusion syndrome, other perinatal hemorrhagic events, and insufficient intake of dietary iron during early infancy. Delayed clamping of the umbilical cord (approximately 120–180 seconds after delivery) can improve the amount of iron and significantly reduce the risk of IDA [24].
Deficiency of iron during pregnancy increases the risk of iron deficiency in the infancy. A study of Kumar et al. showed that iron in the cord blood sample was in correlation with mother’s hemoglobin and ferritin levels [25]. The content of iron in breast milk was reduced in mothers with severe anemia, but it was normal in mothers with mild or moderate anemia. It is recommended to implement iron supplementation during pregnancy in the populations with high prevalence of maternal IDA. It is also important to provide different kinds of iron-fortified foods for pregnant women who are at risk to develop IDA [26].
Prematurity is one of the risk factors for IDA because premature infants have smaller total blood volume at birth compared to healthy term infants, decreased ferritin concentrations, poor gastrointestinal absorption, and increased blood loss through phlebotomies [27]. Iron is mostly accumulated during the third trimester of gestation that is shorter in preterm infants. There is also increased risk for iron deficiency after use of erythropoietin for the prevention and the treatment of the anemia of prematurity [23].
Chronic fetal-maternal hemorrhage and twin-twin transfusion syndrome (TTTS) can reduce iron stores and cause anemia in term or premature infants. A small amount of fetal blood (<0.1 ml) is commonly found in maternal circulation. Causes of increased loss of fetal blood into the maternal circulation are seen as a result of trauma, placental abruption, or may be spontaneous and idiopathic. Manifestations of fetal-maternal hemorrhage depend on the amount and the rapidity of blood loss [28]. TTTS is a rare complication of monochorionic twins (or higher multiple gestations). It is the result of blood transfusion from one twin (donor) to another twin (recipient) through placental vascular anastomoses. The donor twin is smaller and often anemic, and the recipient twin is often plethoric with hemoglobin differences greater than 5 g/dl. Advanced stages of TTTS have 60–100% mortality rate, and fetuses who survive are at risk of severe cardiac, neurologic, and developmental disorders [29].
Feeding and all dietary aspects are very important in early infancy and childhood because they can greatly impact development of IDA. There are many dietary factors that can affect iron metabolism. The most common factors are poor iron intake, decreased iron absorption, consumption of unmodified cow’s milk before 12 months of age, and occult intestinal blood loss due to cow’s milk protein-induced colitis [30].
Poor iron intake in infancy usually occurs when babies are fed with infant formulas or transitional foods which are not fortified with iron. In the study from Chile, the prevalence of IDA was higher in infants fed with the formula without iron (20%), much lower in those fed with iron-fortified formula (0.6%), and medium in infants fed with human milk (15%) [31]. In another study, an increased prevalence of IDA in infancy was observed in infants fed with nonformula cow’s milk > 600 ml or more daily or > 6 breast feeds per day [32]. The amount of iron in human milk is highest during the first month of life, but gradually decreases in the following period. This amount varies among individuals. Maternal diet does not affect iron amount in the human milk.
Intestinal iron absorption depends on the form of iron in the foods. Dietary sources of heme iron, such as fish, meat, and poultry, have higher bioavailability of iron compared to nonheme sources of iron, such as fruits, vegetables, and grains. There are also various components of food that influence intestinal iron absorption. Vitamin C increases iron absorption from bread, cereals, fruits, and vegetables (nonheme iron) but has little effect on the absorption of heme iron. IDA is a common problem in children who follow a vegetarian diet. Intestinal absorption of ferrous and ferric iron is inhibited by tannins in different kinds of teas, foods rich in phosphates, oxalates, carbonates, and phytates (seeds and grains). Purified heme is absorbed poorly because heme polymerizes into macromolecules. Globin prevents the formation of insoluble heme polymers so that it remains available for absorption. Peptides from the degraded globin bind to iron and prevent iron polymerization and precipitation. Different forms of iron can be absorbed better when given together (i.e., spinach with meat).
One of the most important risk factors for IDA is early introduction of unmodified (nonformula) cow’s milk. It increases the risk for intestinal blood loss in infants compared with the formula or breast feeding, mainly due to colitis [33]. Daily intake of 720 ml or more of cow’s milk in preschool children is associated with increased risk for iron deficiency. The reasons are low concentration of iron in cow’s milk, low bioavailability of iron, and possibly increased intestinal blood loss [34]. Sutcliffe et al. reported increased risk for iron deficiency in children with continued bottle-feeding compared with children with cup-feeding in the age of 2–3 years, mainly due to the greater volumes of cow’s milk in bottle-feeding [35].
Dietary iron is absorbed mainly throughout duodenum. Gastrointestinal malabsorption of iron occurs in diseases that affect this portion of the intestine, including celiac disease, Crohn disease, giardiasis, and resection of the proximal small intestine. In children, anemia secondary to iron, folic acid, and vitamin B12 malabsorption is a common complication of celiac disease, and further screening with tissue transglutaminase antibodies has been strongly recommended [36]. Conditions that cause gastrointestinal blood loss are also associated with iron deficiency. These include cow’s milk protein-induced colitis, inflammatory bowel disease (IBD), duodenal/gastric ulcers, and chronic use of nonsteroidal anti-inflammatory drugs or aspirin. Iron deficiency occurs in about 60–80% of patients with IBD. Anemia of chronic disease, vitamin B12 deficiency, folic acid deficiency, and hemolysis contribute to the development of anemia in patients with IBD [37, 38].
Routine screening for IDA should be obtained in children 6–24 months of age. Screening consists of reviewing risk factors during any possible occasion or visit (risk assessment), and laboratory testing (laboratory screening) at least once during the mentioned period. Screening is recommended at all times for all infants and children who have any risk factor (malnutrition, low birth weight, prematurity, signs and symptoms of IDA, or living in the area with high prevalence of iron deficiency).
Review of risk factors in all children is recommended at 4, 15, 18, 24, and 30 months, at 3 years, and once yearly afterward. This is currently the most important and valuable screening tool, more useful than laboratory testing of hemoglobin. Risk assessment consists of focused dietary history. The most vulnerable groups are children with the history of prematurity or low birth weight, infants using low-iron formula, nonformula cow’s milk, soy milk or goat’s milk before 12 months of age, infants having less than two iron-rich meals daily after 6 months of age, preschool children drinking more than 600 ml milk per day, or having less than three iron-rich meals daily.
American Academy of Pediatrics (AAP) suggests laboratory testing as the screening tool for iron deficiency at 1 year of age [30]. Universal laboratory screening is recommended for all children 9–12 months of age. Additional laboratory screening is recommended for children with risk factors for iron deficiency and IDA. There are two groups of children that should undertake additional laboratory screening:
children with high risk for iron deficiency—repeated laboratory testing at 15–18 months of age or when some risk is identified; and
children with special health needs (chronic diseases, inflammatory disorders, restricted diets)—repeated laboratory testing in the period of early childhood (2–5 years of age).
Laboratory screening in most cases includes complete blood count, which includes hemoglobin, hematocrit, mean corpuscular volume (MCV), and red blood cell distribution width (RDW). The minimum laboratory screening is measurement of hemoglobin with the normal value greater than 11 g/dl.
Laboratory testing of serum ferritin at the time of the first screening is the major diagnostic tool in children with risk factors for iron deficiency and IDA [30]. Ferritin levels should be always evaluated carefully because ferritin is nonspecifically elevated in a wide variety of inflammatory conditions. A C-reactive protein can help to validate the results of serum ferritin levels. Other screening measurements that can be taken into account as a different approach for iron deficiency include reticulocyte hemoglobin concentration and combination of soluble transferrin receptor and hemoglobin [39].
It is recommended by AAP to perform risk assessment once a year during the period of adolescence. Adolescents with risk factors (those with a history of IDA, low-iron diet, or girls with heavy menstrual bleeding) should have laboratory testing for anemia [40]. Considering different opinions on screening recommendations in adolescents, each physician should personally decide about the screening process based on the risk factors. Laboratory testing should be done every 5 years starting from age 13 in girls, and at least once during the rapid growth period in boys. Children with any risk factor (increased physical activity, special diets, obesity, malnutrition, chronic illnesses, and heavy menstrual bleeding in girls) should be monitored more frequently [12].
There is some controversy on routine screening for iron deficiency in areas with low rates of iron deficiency and IDA (i.e., United States). Studies provide little evidence that routine screening or iron treatment improves child’s growth and neurodevelopmental outcome. On the other hand, routine screening is recommended because of the important health benefits. Besides, a physician should not decide about screening program only based on symptoms and risk factors in a child. Those who favor screening for iron deficiency in the adolescent period list high prevalence of anemia in that population and adverse consequences of iron deficiency [41]. The screening tests are generally minimally invasive (blood sample), and therapy for IDA is safe.
Many recommendations for prevention of iron deficiency and IDA have been published, and the most commonly used are those provided by WHO and AAP. Widely used approaches include iron-fortified foods in a diet, iron-rich formulas, introduction of cow’s milk in a diet from 12 months of age, screening for iron deficiency, and iron prophylaxis in infants [30].
It is important to emphasize that only a fraction of dietary iron is absorbed from food, depending on bioavailability (dietary iron absorption). Human milk contains only 0.3–1.0 mg/l of iron, but the bioavailability of iron is 50%, while milk formulas contain 12 mg/l of iron with bioavailability of iron 4–6% only [42]. As mentioned above, dietary iron has two main forms: heme and nonheme iron. Plants and iron-fortified foods contain nonheme iron only, whereas meat, seafood, and poultry contain both heme and nonheme iron. Heme iron has higher bioavailability than nonheme iron. The bioavailability of iron is approximately 14–18% from mixed diets, and 5–12% from vegetarian diets. Daily iron requirements vary depending on age and gender. Requirements for iron are 0.6 mg/day in healthy infants and 0.8 mg/day in preadolescent children. Adult males need 1 mg/day of iron, and adult females need 1.5 mg/day [43]. The recommended dietary iron for healthy full-term infants (from birth to 12 months of age) is 1 mg/kg/day (maximum 15 mg); for premature infants 2–4 mg/kg/day (maximum 15 mg); for toddlers 1–3 years of age 7 mg/day; for children aged 4–8 years 10 mg/day; for children aged 9–13 years 8 mg/day; for adolescent boys aged 14–18 years 11 mg/day, and for adolescent girls aged 14–18 years 15 mg/day [43]. Boys have increased requirements during pubertal growth because of expanding blood volume and increase in hemoglobin concentration. Increased requirements in girls during puberty are mostly due to menstrual blood loss, although the loss differs in various individuals. Besides, adolescent girls more often have a tendency to eat food that contains less iron and to avoid high iron-containing foods, contributing to iron deficiency [44].
Infants who are not breastfed, obtain sufficient amount of iron from iron-fortified formula. Breastfed infants should receive an additional source of iron (as iron supplement or complementary food) in these doses:
Full-term breastfed infants should receive an iron supplement from the age of 4 months (1 mg/kg/day, maximum 15 mg) until the infant has sufficient iron-rich complementary foods in a diet.
Premature breastfed infants should receive an iron supplement starting from the age of 2 weeks (2–4 mg/kg/day, maximum 15 mg) throughout the first year of life (as supplements or iron-fortified formula).
Supplementation of iron is necessary to meet requirements in infants from populations with high rates of iron deficiency and IDA. In a prospective randomized trial of early versus late iron supplementation in low-birth-weight infants, infants who received early iron supplementation (started when feedings reached 100 ml/kg/day) had lower risk of infection and lower number of blood transfusions compared to infants who received late supplementation (started at 61 days of age) [45]. In a study from India that included breastfed infants at the age of 4–6 months, oral iron supplementation resulted in better growth, especially in infants who had anemia or were otherwise nutritionally deficient [46].
Prevention of iron deficiency and IDA varies by geographical region, age group, and other conditions. In countries with high prevalence of IDA, comprehensive strategies and interventions for high-risk groups are implemented, in particular for young children, adolescent girls, women in reproductive age, and pregnant and breastfeeding women. In some regions, food fortification with iron, control of helminth infection, and control of malaria are effective approaches to prevent IDA [17].
The optimal way to reach iron requirements is an improvement of food quality. In countries with low prevalence of iron deficiency, recommended dietary intake should assure expected iron requirements. Exclusive breastfeeding is recommended for the first 4–6 months of life. Preterm breastfed infants should receive an iron supplement from 2 weeks of age. Additional source of iron should be given to infants starting at 4 months of age, first as an iron supplement, followed by iron-fortified foods (two or more meals/day meet the expected requirements for iron). Partially breastfed and nonbreastfed infants should consume exclusively iron-fortified formulas [47].
Starting from the age of 6 months, infants should receive one feeding rich in vitamin C (green vegetables, fruits, and juices) daily. After 6 months of age, meat should be introduced in a diet. Heme iron (meat and fish) is more bioavailable than nonheme iron (vegetables and cereals). Combining heme foods with nonheme foods also increases the absorption of iron [48]. Moreover, consumption of meat meets many requirements besides iron.
Infants should not be given nonformula cow’s milk until the age of 12 months. The higher concentration of calcium in cow’s milk inhibits absorption of iron. Children aged 1–5 years should drink less than 600 ml of milk daily. Besides, they should take enough iron-containing foods to fulfill daily iron requirements. Children, who do not eat at least 2 or 3 iron-rich foods every day, may have inadequate iron intake and may need iron supplementation [49].
IDA is the final stage of iron deficiency, and the first one that can recover with iron supplementation. Iron deficiency without anemia may also be associated with some clinical signs and symptoms, such as fatigue, cognitive dysfunction, or decreased energy.
The most common presentation of IDA in an asymptomatic infant or a child, who is well-nourished and otherwise healthy, is mild-to-moderate microcytic and hypochromic anemia. Slowly progressive paleness may sometimes be missed, but anemia also produces nonspecific pallor of the mucous membranes. Signs of epithelial tissues that may be associated with IDA are koilonychia, glossitis, and angular stomatitis. Severe form of IDA is much rare and is presented with poor feeding, irritability, lethargy, tachypnea, and cardiomegaly. Growth is impaired in children with severe IDA, and splenomegaly may be present.
Symptoms of IDA are presented by many body systems and functions of the affected child: impaired psychomotor and/or mental development, effects on immunity and susceptibility to infection, decreased exercise capacity, weakness, pica and/or pagophagia, headache, irritability, beeturia, and restless leg syndrome in older children. Some of these symptoms may lead to long-term consequences. Iron deficiency significantly contributes to thrombotic risk. In cases of severe IDA, some children may experience acute life-threatening conditions, including hypotension, tachycardia, tachypnea, respiratory distress, and congestive heart failure. The presence of one or more of these findings requires immediate hospital admission and prompt treatment. Severe IDA may rarely be associated with increased intracranial pressure, clinical signs of pseudotumor cerebri, or papilledema. All these symptoms resolve with iron supplementation [50].
Impaired psychomotor and/or mental development is common in infants with iron deficiency, and neurocognitive impairment in adolescents with IDA [51–53]. Negative impact on social and emotional behavior may appear and can lead to the development of attention deficit hyperactivity disorder (ADHD) [54]. Mood swings are frequent. Children with iron deficiency get tired easier and faster, and play less compared to healthy children. Numerous randomized trials performed on different pediatric age groups showed that iron supplementation prevented or corrected neurodevelopmental delay. These studies were mostly performed in low- or middle-income countries [55–57]. In the study from Costa Rica, iron deficiency and IDA were more frequent in infants fed with nonfortified- iron formula. In these infants, psychomotor development declined at the age 9 and 12 months. There were not any significant changes in mental development and behavior [58]. Some other studies demonstrated that psychomotor impairment might not completely recover after treatment of moderate-to-severe IDA [56, 59–62]. Children who had iron deficiency at the inclusion in the study continued to have lower cognitive scores when tested at school age and in adolescence compared to children with good iron balance and no iron deficiency [59]. Children who were treated for iron deficiency during infancy had lower scores on electrophysiological tests on recognition memory at 10 years of age, comparing with children without iron deficiency during infancy. Behavioral tests showed similar results in these two groups [61].
The biologic basis of neurodevelopmental disorders is not fully understood. Iron deficiency decreases expression of dopamine receptors, disrupts function of several enzymes in the nervous system with subsequent alterations in brain energy, and decreases myelin formation. Myelination disruption or impairment can be associated with constant changes in transmission through auditory and visual systems. In a study from Chile, auditory brainstem responses (ABR) and visual evoked potentials (VEP) were measured in two groups of 4-year-old children: children who were treated for IDA in infancy and non-anemic children who also received iron supplementation [63]. Subtle auditory and visual dysfunction was demonstrated with longer VEP and ABR latencies in children who had IDA in infancy compared with control group.
The relationship between IDA and febrile seizures (FS) has been examined in several studies with conflicting results. Studies that suggest positive correlation between iron deficiency and FS aim that the possible mechanism is iron-dependent metabolism of some neurotransmitters [64, 65]. Other studies found no association between iron deficiency and FS [66]. Zehetner et al. showed that iron supplementation for 16 weeks in dosage 5 mg/kg/day reduced the severity and frequency of breath-holding spells in children with IDA [67].
Iron deficiency and IDA have numerous effects on immune system and susceptibility to infection. Iron deficiency in children can induce defective functions of leukocytes and lymphocytes, and defective production of interleukin (IL)-2 and IL-6 [68, 69]. On the contrary, iron overload can increase the risk of infections with specific types of bacteria. Accumulation of iron in immune cells interferes with their antibacterial activity, and some bacteria grow well in an iron-rich environment. Besides, iron-binding proteins transferrin and lactoferrin have bacteriostatic effects, and these effects are lost when these proteins are saturated with iron [70].
Since both iron deficiency and iron excess can compromise cellular function, the levels of iron that cells are exposed to should be regulated precisely. In populations with high prevalence of iron deficiency and IDA, iron supplementation has different effects on susceptibility to infection and immunity. Low iron status may protect against malaria infection, but malaria in turn is linked with anemia, and changes in iron metabolism during a malaria infection may modulate susceptibility to co-infections [71]. Recent study of Zlotkin and coworkers showed that iron supplementation did not increase the risk of malaria infection [72].
Iron is an essential cofactor in aerobic metabolism. In IDA muscles are forced to depend on anaerobic metabolism more than they do in healthy nonanemic individuals. Iron deficiency leads to decreased exercise capacity in children, especially adolescent athletes. IDA is associated with decreased work capacity [73, 74].
Pica refers to unusual appetite for substances that are not food. In children, pica is often associated with iron deficiency and IDA [75]. The most common form of pica is starch or clay ingestion. Both substances decrease absorption of dietary iron. Pagophagia is a particular form of pica characterized by repetitive and compulsive ingestion of ice, freezer frost, or iced drinks. Some children prefer cold vegetables instead of ice. Pagophagia is very common in iron deficiency without anemia and is present in a half of patients with IDA. It responds to iron supplementation very fast, earlier than hemoglobin recovery [76]. The mechanism through which iron deficiency causes pagophagia is unclear. Biochemical processes involving the central nervous system might elucidate the underlying mechanism. Pica is not specific for iron deficiency. It can be found in children with developmental disabilities, such as intellectual disability or autism. It is also described in children after brain injury [77].
Both iron deficiency and overload have been associated with an increased thrombotic risk in experimental and clinical studies. It has been reported that IDA is associated with cerebral vein thrombosis [78]. In Canadian study, children with arterial or venous stroke who were previously healthy, had ten times more chance to have IDA than children without stroke [79]. The mechanism of this association is complex. It may be related to reactive thrombocytosis that is often finding in IDA. Iron deficiency may contribute to a hypercoagulable state by affecting blood flow patterns. Besides, IDA with hypoxia could precipitate situations of increased metabolic stress (i.e., infections) in particularly vulnerable areas of the brain supplied by end arteries [80].
Beeturia is defined as pink or red urine after the ingestion of beets. It is most common in individuals with iron deficiency [81]. This manifestation is caused by increased intestinal absorption and increased excretion of the red pigment betalaine (betanin). The pigment is decolorized by ferric ions, and urine excretion of betalaine is increased in iron deficiency.
This syndrome is a common sleep-related movement disorder characterized with uncomfortable urge to move legs. It occurs usually in the evenings, during periods of inactivity and rest, and is occasionally relieved by movement. Restless leg syndrome is associated with iron deficiency and is often improved by iron supplementation. The brain iron insufficiency has been documented by independently replicated cerebrospinal fluid and brain imaging studies for individuals without IDA [82].
Detailed history and physical examination are essential in diagnosis of any disease. Detailed history from the parents is very important in diagnosing iron deficiency and anemia, especially about prenatal period and dietary habits including time of introducing solid foods.
Presumptive diagnosis of IDA is made by a combination of risk assessment and laboratory testing of hemoglobin level (<11 g/dl). In infants younger than 6 months, lower values of hemoglobin are observed because of physiological anemia, but hemoglobin values under 9 g/dl demand further evaluation in order to investigate if there is any accompanying factor. Other findings like low mean corpuscular volume (MCV) or high red cell distribution width (RDW) help to determine diagnosis. For a definite confirmation, additional steps are needed:
Estimate risk factors for lead poisoning and measure blood lead level if it is indicated [30, 83].
If there is no evidence of lead toxicity, and the most likely is dietary deficiency, apply empirical trial of oral iron supplementation*
For infants and toddlers less than 24 months of age with anemia—move directly to empirical trial because IDA is the most probable cause of anemia in this age group.
For children 24 months of age and older—besides hemoglobin, hematocrit, MCV, and RDW, evaluate reticulocyte count, peripheral blood smear, and stool for occult blood before starting empirical trial.
In children with severe anemia, complicated medical history, and with signs and symptoms atypical for IDA, additional testing should be performed before starting treatment.
These additional steps are necessary because anemia is not sensitive or specific for iron deficiency. Two-thirds of children with iron deficiency in the United States are not anemic, namely 9% have iron deficiency and 3% are anemic. The prevalence of anemia is much higher in countries with higher rates of iron deficiency. On the other hand, two-thirds of anemic toddlers have some other cause of anemia apart from iron deficiency [30]. Evaluation for iron deficiency in adolescence should also include serum ferritin levels. IDA in adolescent is identified by hemoglobin concentration below 11 g/dl combined with low serum ferritin (<12 ng/ml).
In infants and toddlers up to 24 months of age who have mild microcytic anemia with presumptive diagnosis of IDA based on screening results, the strategy of choice is therapeutic trial of iron [51]. The recommended dosage is 3 mg/kg of elemental iron, once or twice daily, best between meals (daily dosage 3–6 mg/kg). Ferrous sulfate is the convenient and most commonly used form of iron. If there is increase of hemoglobin concentration greater than 1 g/dl after 4 weeks of treatment, the diagnosis of iron deficiency is confirmed. In this case, iron supplementation and monitoring of the child with laboratory tests should be continued for at least several months, after hemoglobin levels reach normal range according to age.
IDA is less common in older children than in infants. Additional evaluation, besides complete blood count, MCV, and RDW, is suggested in children older than 2 years before starting iron treatment. This evaluation includes reticulocyte count, peripheral blood smear, and stool for occult blood. If results support the diagnosis of IDA, iron supplementation should be started. Additional evaluation is required only if there is no response to the treatment.
Basic laboratory testing in diagnosing IDA is complete blood count, including hemoglobin, hematocrit, MCV, and RDW. More detailed evaluation is needed for children with complicated medical histories, severe forms of anemia (hemoglobin <7 g/dl) or presence of features that are not typical for IDA. In these cases, several other tests should be performed: serum iron, serum ferritin, total iron-binding capacity (TIBC), transferrin saturation, and stools for the presence of occult blood. These tests, although nonspecific for IDA, can support the diagnosis of IDA in majority of cases. Low serum iron and ferritin levels with an elevated TIBC are diagnostic for iron deficiency.
Complete blood count shows the severity of anemia. Increased RDW is the first laboratory sign of iron deficiency [51, 84]. RDW is high in IDA because there is a wide variation in RBC size. MCV and mean corpuscular hemoglobin concentration (MCHC) are low. Platelet count is often elevated, and it normalizes after iron treatment. Peripheral blood smear is an important workup in patients with anemia. The first finding of IDA on peripheral smear is anisocytosis. Besides, RBCs are hypochromic and microcytic.
In infants and small children, iron deficiency is usually identified by a serum ferritin concentration <12 ng/ml. Diagnosis of IDA is based on the combination of hemoglobin concentration below 11 g/dl and serum ferritin levels below 12 ng/ml. However, when examining the results, it must be taken into consideration that ferritin is an acute-phase reactant. Elevated serum ferritin levels have been associated with a wide range of conditions including inflammation, infection, chronic disease, and malignancy [85].
Free erythrocyte protoporphyrin (FEP), soluble transferrin receptor (sTfR), and reticulocyte hemoglobin content (CHr) are very useful and reliable laboratory tests to support the diagnosis of iron deficiency. FEP is a precursor of heme that normally occurs in very low concentration in RBCs. Elevated FEP values thus indicate early impairment of iron status and provide information about gradual changes in the iron supply. The sTfR refers to the cleaved extracellular portion of the transferrin receptor 1 that is released into serum. Iron deficiency causes overexpression of transferrin receptor and sTfR levels. The sTfR is regarded as a more stable marker of iron levels in an inflammatory state. CHr is a measure of early iron-deficient erythropoiesis. Reticulocyte hemoglobin content decreases earlier than hemoglobin content of RBC because normal life span of RBC is 120 days [86]. It has been shown that CHr measurement is more reliable and accurate laboratory test for the diagnosis of iron deficiency than hemoglobin level <11 g/dl, resulting in detection of greater number of patients with iron deficiency comparing to hemoglobin. On the other hand, greater number of falsely identified patients with iron deficiency was detected also by CHr, which is, although more sensitive, less specific than hemoglobin [87]. Serum transferrin receptor is found on reticulocytes and increased number of transferrin receptors is observed in IDA.
Some other types of anemia and other conditions that can be confused with IDA are mild hereditary anemias (alpha or beta thalassemia traits), mild anemia after recent infection or immunization, anemia of chronic disease, and combined nutritional anemias (malabsorption with vitamin B12 or folate deficiency). If the child does not respond to iron supplementation nor has some predisposing factor, other conditions should be considered.
For the successful treatment of IDA in infants and children, it is necessary to determine the appropriate dose and scheduling of oral iron therapy, apply dietary modifications together with iron supplementation, and follow-up the response to treatment.
Suggested dose for oral supplementation for infants and children with IDA is 3–6 mg/kg/day of elemental iron. Ferrous sulfate is generally recommended in a dose of 3 mg/kg of iron once or twice daily (maximum total daily dose, 150 mg of elemental iron). Elemental iron constitutes 20% of ferrous sulfate. Ferrous fumarate and ferrous gluconate are other forms of oral iron salts with different content of elemental iron. The iron supplement should be given between meals and preferably with juice because absorption of ferrous sulfate is increased when it is given with juice rather than with milk or other fluids. For maximum absorption of iron, administration 30–45 minutes before meal or 2 hours after meal is highly recommended.
The same doses of oral iron supplementation are recommended as a therapeutic trial for infants and young children with mild microcytic anemia and presumptive diagnosis of IDA [51]. Treatment should result in an increase of hemoglobin concentration greater than 1 g/dl within 4 weeks [30].
Side effects of oral iron preparations are gastrointestinal intolerance in higher doses, gray staining of teeth and gums (especially when given as a liquid preparation), effects on immune system, and susceptibility to infection.
Dietary changes are necessary not only to prevent iron deficiency but also to add oral iron therapy. Following dietary changes are recommended for infants and children with proven or suspected IDA:
Infants should not be fed with unmodified cow’s milk or low-iron formula. If infants are not breastfed or are partially breastfed, they should be fed with iron-fortified formula. Infants fed with cow’s milk may have iron deficiency as a result of intestinal blood loss due to cow’s milk protein-induced colitis. Lack of iron fortification in unmodified cow’s milk contributes to iron deficiency state.
When iron deficiency is detected or suspected in a child older than 12 months, intake of cow’s milk should be limited to 600 ml/day. Higher intake of cow’s milk has been associated with higher risk for iron deficiency in several studies [34, 88]. Discontinuing bottle-feeding is also recommended because it generally helps in limiting milk intake [89]. If IDA is persistent and stool is positive for blood, all milk products should be stopped. In these cases, child should receive appropriate amount of calcium in a diet (calcium-rich foods).
Parents should be advised to modify child’s diet in order to increase iron consumption. Infants 6 months and older should have appropriate intake of iron from complementary foods. Diet should contain cereals fortified with iron, food rich in vitamin C, and pureed meat.
Follow-up assessment is necessary to confirm that anemia has been caused by iron deficiency and the treatment was administered at correct dosage and timing. After 4 weeks of therapy, complete blood count should be done. It is recommended to perform evaluation when child is healthy and without viral infection that may cause acute decrease in hemoglobin.
If hemoglobin has increased at least by 1 g/dl after 4 weeks of oral iron supplementation, therapy should be continued, and hemoglobin re-evaluated every 2–3 months until hemoglobin reaches the normal value. Iron therapy should be continued additional 2–3 months to replace iron storage pools. Discontinuation of the treatment can lead to the recurrence of IDA.
If the appropriate response is missing after 4 weeks of treatment, additional evaluation of anemia is recommended. Possible causes of persistent or recurrent IDA are ineffective treatment, blood loss, malabsorption, or incorrect diagnosis. Parents should be asked whether the iron preparation has been given at the appropriate dosage and timing, whether suggested dietary modifications have been done, and if there were any intercurrent illnesses that could transiently decrease hemoglobin level. If the patient had no intercurrent illness and has been taking iron supplement in an appropriate dosage and timing, it is suggested to proceed with the following evaluation:
Evaluation for the type of anemia—Measuring of serum ferritin level, hemoglobin electrophoresis, vitamin B12, and folate can rule out the thalassemia trait, chronic disease anemia, and mixed nutritional deficiency. These conditions may imitate or complicate IDA. Very rare genetic mutations may interfere with iron transport and cause anemia similar to IDA, but without response to iron supplementation [90].
Evaluation for gastrointestinal blood loss—Stool should be tested for occult blood in a few separate samples. If the results are positive, it is recommended to assess further investigation for common causes of gastrointestinal blood loss, including cow’s milk protein-induced colitis, celiac disease, and inflammatory bowel disease.
Parenteral iron therapy is reserved for patients with severe forms of anemia who are intolerant to oral preparations, have poor response to oral supplementation, poor compliance, or malabsorption. Children with chronic gastrointestinal diseases as inflammatory bowel disease may require parenteral iron therapy because they often do not tolerate oral supplementation.
Most commonly used form of iron for parenteral use in children is low molecular weight iron dextran. It produces mild infusion reactions in less than 1% of patients and serious adverse effects are very rare [91]. Recently, ferric carboxymaltose administered as a short intravenous infusion without a test dose proved to be safe and highly effective in children and adolescents with IDA refractory to oral iron therapy [92]. Evaluation of treatment is usually performed at 4–12 weeks after the initial infusion.
Blood transfusion is rarely required in children with IDA. Transfusions are not considered necessary even with hemoglobin levels 4–5 g/dl, if the child is otherwise well. Blood transfusion should be administered only when there is an urgent need to restore oxygen-carrying capacity, i.e., in severe decompensated anemia. IDA develops gradually and over periods long enough to allow compensatory mechanisms to maintain intravascular volume. Consequently, there is a real risk of fluid overload with transfusion, and these patients should receive transfusion with caution. Standard of practice recommends slow transfusion of packed RBC volume of 5 ml/kg over 4 hours to avoid complications [93].
Iron deficiency is the most common nutritional deficiency in the world, affecting more than a quarter of the global population. Iron plays an essential role in many physiological functions, including oxygen binding and transport, cell growth and differentiation, gene regulation, enzyme reactions, and neurotransmitter synthesis. Iron deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases compensatory. During later stages, deficiency impairs erythropoiesis, ultimately causing anemia.
Iron deficiency and IDA have many systemic effects, and the most concerning are diminished mental, motor, and behavioral functioning that might not be completely reversible after treatment with iron. Therefore, intervention should focus on primary prevention, which includes breastfeeding, fortification of foods with iron, use of iron-rich formulas when breastmilk is insufficient, and avoiding cow’s milk before 1 year of age. Routine laboratory screening is recommended for all children 9–12 months of age. Risk assessment, consisting of focused dietary history, presents the most valuable screening tool, and additional laboratory screening is recommended for children with risk factors for iron deficiency and IDA.
Treatment starts with establishing the diagnosis. The main therapeutic principles are detection of the condition that causes iron deficiency, correction of underlying etiology, iron supplementation, dietary modifications, and education of families. Oral iron is the first-line therapy, giving in appropriate dose and scheduling. Adequate follow-up assessment for response is also important. If the appropriate response is missing, further evaluation should be obtained to rule out conditions that might simulate or complicate IDA.
WHO | World Health Organization |
IDA | Iron deficiency anemia |
BMI | Body mass index |
RBC | Red blood cells |
TTTS | Twin-twin transfusion syndrome |
IBD | Inflammatory bowel disease |
AAP | American Academy of Pediatrics |
MCV | Mean corpuscular volume |
RDW | Red blood cell distribution width |
ADHD | Attention deficit hyperactivity disorder |
ABR | Auditory brainstem response |
VEP | Visual evoked potential |
FS | Febrile seizures |
IL | Interleukin |
TIBC | Total iron-binding capacity |
MCHC | Mean corpuscular hemoglobin concentration |
FEP | Free erythrocyte protoporphyrin |
sTfR | Soluble transferrin receptor |
CHr | Reticulocyte hemoglobin content |
In the past decades extensive research and development (R&D) has made for effective protection of the occupants in conventional vehicles. Through analytical and experimental investigations on the kinematics response and injuries of postmortem human subject (PMHS) in forward-facing seating under different frontal, oblique, side, and rear impacts, the injury measures and criteria for the trauma of each body region at Abbreviated Injury Scale (AIS) with the injury risk probability function have been defined. The families of the anthropomorphic test devices (ATDs) have been developed as the laboratory test tools for surrogate human occupants representing a population of different gender and ages. These ATDs included advanced THOR dummies for the 50th%ile adult male and 5th%ile female and Hybrid-III dummies for 95th%ile and 50th%ile adult males, 5th%ile female, 10 year old, 6 year-old, 3 year-old, and 1 year children, mainly for the frontal impact applications; WorldSID, Eurosid, US-Sid dummies of the 50th%ile male and 5th%ile female for the side impacts; and BioRid dummy for the rear impacts. Dummy based measures and criteria for the human body injuries have been developed from the paired studies of the PMHS tests and dummy tests at laboratory impact test conditions.
Based on the research and development, the government regulatory crash tests and evaluation standards known as New Car Assessment Programs (NCAP) and other motor safety regulations have been implemented in industry for nearly three decades, mainly for occupant protection of the forward-facing seated occupants in conventional vehicles, including the first-row driver and passenger and the second-row occupants, for vehicle frontal, side and rollover crashes. It was estimated to have saved hundreds of thousands of lives in the field each year [1].
As new automated vehicles technologies are accelerating in recent years, the National Highway Traffic Safety Administration (NHTSA) [2] released new federal guidance for Automated Driving Systems (ADS) on September 12, 2017, prioritizing occupant safety with the vision for safe deployment of automated vehicle technologies to a future with fewer traffic fatalities and increased mobility for all occupants. The new guidance supports further development of this important new technology, and offers a voluntary guidance for twelve priority safety design elements of the ADS, including new occupant protection systems that provide enhanced protection to occupants of all ages and sizes, additional countermeasures that will protect all occupants in any alternative planned seating or interior configurations, and the tools to demonstrate such due care not only limited to physical testing but also including virtual tests with vehicle and human body models.
Automated vehicles (AV) will pose challenges and opportunities for occupant protection since an AV could involve in different crash conditions, occupants could be from more diverse population, and seating arrangements could be free of restriction.
Recent trends in AV interior seating configurations bring more innovative and versatile design options than the conventional vehicles. In additional to the traditional forward-facing seats, AV seating designs may consider oblique-facing, rear-facing, and side facing or any other angle-oriented seating positions. The occupant postures in an AV could also vary at great extent, from normal seated to leaning backward until lying down. Jorlöv, S. et al. [3] investigated user desires and attitudes to seating positions and activities in future highly automated cars. The survey found that during long drives, with several occupants in the car, there is a desire to rotate the seats to a living room position. During shorter drives alone, users would prefer to maintain the forward-facing position, but with the seat reclined to a more relaxed position.
For effective protection to all occupants of all ages and sizes in any alternative planned seating or interior configurations from various vehicle crashes, it is necessary for us to understand better the kinematics and injury patterns and outcomes of AV occupants at new seating configurations, and to develop better biofidelic tools and occupant injury evaluation methods.
In the past several years some fundamental biomechanics research has been performed on the PMHS and dummies in oblique facing, rear facing, and side-facing seating positions and reclined postures. Jason et al. [4] studied kinematic occupant responses and injury outcomes from 3-point seatbelt restrained PMHS in a forward-facing seat subjected to lateral and oblique far-side vehicle crash pulses of 6.6 mph and 14 mph. Humm, J.R., et al. [5] studied kinetic and kinematic occupant responses, and injury outcomes from the lap-restrained PMHS in the oblique and side-facing seats subjected to a frontal pulse with 16 g peak, 13.4 m/s (48 km/h or 30 mph) change in velocity, and 90 ms rise time (USCFR-1988) in an aviation environment. The sustained injuries included spinal injuries for all subjects varying with vertebral level, rib fractures, pelvic injuries, and leg injuries. Kang et al. [6, 7] studied kinematic responses and injury outcomes from the 3-point seatbelt restrained PMHS in the rear-seats subjected to frontal pulses of 16 mph, 24 mph and 35 mph crash severities of a represented vehicle. Minor c-spine injuries and transverse process fractures, 3–15 ribs fractures were observed from the PMHS at the rear seat under the 35 mph crash pulse. More injuries (Clavicle, scapula, and pelvis fractures) were observed from the PMHS at same test condition with the reclined 45 deg. seating.
Good progress has also been made in development of omni-directionally biofidelic human body models (HBMs). In the past decades, several finite element human body models for the occupants and pedestrians have been developed worldwide. Most recently, Global Human Body Model Consortium (GHBMC) have developed a family of HBMs in total of 13 models representing the 95th%ile and 50th%ile male and 5th%ile female occupants and pedestrians, and a six-year old child pedestrian. Biofidelity of the GHBMC 50th%ile male detailed occupant model (M50-O v4.5) was evaluated for the responses to the UVA PMHS farside sled tests condition [8], as well as to the rear impact sled tests by Kang et al. [9]. These results indicated better biofidelity of the HBMs than the dummies at these conditions.
In this research, we have used the GHBMC HBMs as a tool for assessment of the occupant kinematics and injuries, and for evaluation of the restraint performance.
The objectives of this research were the following
to develop the accidental injury risk assessment method with the GHBMC HBMs,
to better understand the body injury patterns and severities for a belted 50th%ile male occupant at various orientated seating positions under a vehicle frontal crash pulse and at a side-facing seating position under frontal, oblique, side, and rear vehicle crashes, and
to develop new concepts of effective restraints for the AV occupant protection.
In this chapter, Section 2 summarizes the GHBMC HBM validations and the occupant injury risk assessment methods. Section 3 states the occupant injury analysis for the seating in various 360 degree orientated seating positions. Section 4 focuses on the occupant injury analysis for the side-facing seat occupant. Section 5 demonstrates the evaluation methods and results for new restraint concepts for protection of the side-facing seat occupants.
In this study we used the GHBMC 50th%ile male occupant human body models in two versions – detailed M50-O v4.5 and simplified M50-OS v1.8.4. The M50-O v4.5 model has 2,187,596 elements and 1,263,445 nodes, while the M50-OS v1.8.4 FE model has 338,814 elements and 299,095 nodes.
The Global Human Body Models Consortium (GHBMC) M50-O average male seated occupant is a widely used and validated HBM. The detailed M50-O v4.5 occupant model has been validated at the tissue, component, and full body crash test levels during the development. GHBMC models were developed from external anthropometry and posture specific medical image data [10, 11]. A multi-modality image dataset from volunteers representing various target anthropometries were used. Over 14 thousand images across three imaging modalities (CT, MRI, and upright MRI) were collected for the M50 model including scans in the supine, standing, and seated postures [12]. Geometries for the M50 were developed from these image datasets using a variety of segmentation techniques. Segmented data were verified against or augmented with data from literature sources [13].
Component level validation has been conducted in each major body region. In the head, the model was validated by comparing the response in matched simulation of impacts to bony structures (e.g. maxilla [14], zygoma 10], nasal bone [15], and skull [16]). Various soft tissue injuries were validated including intracranial pressures [17, 18], and relative brain to skull motion [19, 20]. In the neck, segment level tests were validated using individual functional units [21, 22, 23, 24], functional units and full spine in tension [25], ligamentous strain [26, 27, 28, 29], and axial rotation [30, 31]. The full cervical spine was tested in various configurations including rear impact [32, 33], lateral impact, and frontal impact [34, 35]. The thorax was validated at the rib cage level using a denuded rib cage study [36], pendulum impacts [37, 38, 39], and table top impacts [40]. The individual response of a single rib was the subject of an optimization study [41]. The abdomen was validated in various tests using bar impacts with a free back [42, 43], belt loading with a free back [43], airbag loading with a fixed back [43], belt loading at the mid abdomen [44, 45], pendulum impact [46], organ level validation at impact [47], lumbar flexion [48], lateral impact [49] and side airbag loading [50]. The pelvis was validated in lateral compression at the acetabulum [51, 52, 53] and pubic symphysis [54]. The lower extremity has been validated in various loading conditions including axial loading. The ankle has been specifically studied in impacts for axial loading, ankle inversion, eversion, dorsiflexion, and rotation [55, 56, 57, 58]. Furthermore, the tibia has been validated in a three-point bending setup as well as axial loading for the entire leg [59, 60].
The model has also been extensively validated at the full body level in classical macro-level injury biomechanics studies [61]. Along with validation in dynamic simulations, the mass distribution of the GHBMC M50 model was validated [62] by virtually sectioning the model into body regions and comparing masses to anthropometric PMHS data from McConville et al. [63] and Robbins [64]. Rigid impacts to body regions (e.g. thorax, pelvis, etc.) in frontal, oblique, and lateral directions were applied to the model based on experimental designs in the literature [43, 65, 66, 67, 68, 69]. Care was taken to closely approximate the experiment, including considerations of motion constraints on impactors and the inclusion of gravity, seat backs, etc. Three sled tests in frontal [70, 71] and lateral [72] directions have been validated. An example of these simulations is shown below (Figure 1).
Sample validation using the GHBMC M50 model. Left to right: Shaw et al. sled buck model setup, head Z displacement and lower left rib displacement.
The M50-OS v1.8.3 model provides relevant biomechanical output data from the same body habitus as the detailed model, but at a substantially reduced computational cost. The simplification process included reducing the total number of elements through re-meshing, consolidating contact definitions, utilizing simplified material properties, and implementing kinematic joints throughout the body. The M50-OS model exhibits roughly a 40-fold decrease in run time (Table 1). Since joint definitions and meshes were designed to maximize the ability to position the model, a semi-automated positioning “tree” was programmed into LS-PrePost allowing the user to dynamically adjust joint angles prior to running a simulation.
Test | Detailed Model Run Time (min) | Simplified Model Run Time (min) | Run Time Reduction (Detailed/Simplified) |
---|---|---|---|
Thorax hub impact | 583 | 15 | 38.9 |
Lateral sled impact | 1554 | 40 | 38.9 |
Run time results for the simplified M50 occupant model.
The published work on the M50-OS v1.8.3 model [73] reported thirteen validations and robustness simulations, which included denuded rib compression at 7 discrete sites, 5 rigid body impacts, and one sled simulation. Perez-Rapela, D., et al. [74] compared simulated kinematics in their far-side impact sled tests with the M50-OS v1.8.3 model to the PMHS responses. Results showed that, in general, the model captured lateral excursion in oblique impact conditions but overpredicted in purely lateral impact conditions. The human body model obtained a “good” CORA score for the correlation of their evaluation.
The injury measures are Head Injury Criterion (HIC36 for side and HIC15 for frontal) and Brain Injury Criterion (BrIC) for the head region, Chest Lateral Deflections (side and frontal) for the chest, Abdominal VC for the abdomen, Pubic symphysis peak force for the pelvis, and Femur Force for the KTH region, and Upper Tibia Force and RTI for the lower extremities, respectively. The Full Body Injury Index FBII was defined as a summation of all the body region injury probabilities. Table 2 summarizes these injury measures and the body region injury risk functions.
Injury Type | Injury Measure | Injury Risk Function | Ref. |
---|---|---|---|
Head AIS 3+ | HIC36 (side) HIC15 (Frontal) | [75] | |
BrIC | [76] | ||
Chest AIS 3+ − - Frontal | CD | [77] | |
Chest AIS 3+ − - Side | CD | [77] | |
Abdomen AIS 2+ | VC | [78] | |
Pelvis AIS 2+ | Pubic Force Fp | [79] | |
KTH AIS 2+ | Femur Fz | [80] | |
Tibia AIS 2+ | Upper Tibia Force | [80] | |
Tibia/Fibula Shaft fracture AIS 2+ | Tibia Index RTI | [80] | |
Ankle AIS 2+ | Lower Tibia Fz | [80] | |
Full Body Index | FBII |
The human body region injury risk functions for the 50th%ile male occupant.
In this study, the human occupant injury risks were estimated with these probability functions. The estimations served as comparative measures for the body region injury severities among different analysis cases.
An occupant could be injured at a vehicle crash when the external impact forces on his/her body regions exceed the tolerances. The force magnitude related to the vehicle crash severity and the principal direction of force (PDOF) affect the body region injury patterns and severities. The PDOF could vary for an occupant on a given seating position with different crash scenarios (frontal, oblique, side, or rear impacts to the vehicle), or vary with different seating orientations under one vehicle crash. In the real-world, there are more occurrences of vehicle frontal crashes than other impacts.
Kitagawa, Y., et al. [81] analyzed occupant kinematics in simulated frontal collisions with three speeds assumed (56 km/h, 40 km/h and 30 km/h) using the THUMS Version 4 AM50 occupant human model representing the 50th%ile male occupant seated varying seating orientations with every 45-degree increment from 0 degree (forward-facing) to ±180 degrees (rear-facing) with respect to the impact direction, and with three angles of the seatback from 24 degrees to 36 degrees for two seating positions. The results showed that the occupant had the largest torso lateral excursion (up to 700 mm at a 56 km/h frontal crash) at −45 degrees and − 90 degrees orientated (side-facing) seating positions.
In this study, we focused on analysis of occupant injury patterns and risks for a mid-size male occupant on a seat with the orientations varying to the PDOF 360 degree under a moderate frontal crash pulse.
We simulated a belted mid-size male occupant on a seat in a conceptual automated vehicle subject to the 40 km/h (25 mph) frontal crash pulse from Shaw PMHS golden test [70] as shown in Figure 2 (left graph). The 3-point seatbelt restraint was with pretensioner and 3.5 kN load limiter. Figure 2 (right graph) shows the simulation cases with the GHBMC M50-O v4.5 model representing the male occupant. For each simulation case, the seat was rotated with every 30-degree increment from 0 degree to 360 degrees respect to the frontal impact. It is noted that each case number is named same as the clock number.
The 40 kph (25mph) frontal crash pulse (left graph) and the 50th%ile occupant seating positions considered in this study (right graph).
The models of the seat and seatbelt were used the same as what have been validated from the NHTSA‘s Advanced Adaptive Restraint Program (AARP) [82]. For the seat model, additional validation was made for the rotational stiffness of the seat back against the published body block test data [83], in which the seat back forward-rearward rotation was allowed within +20 degrees.
From the simulations for the twelve cases with the defined different seating orientations, analyses were made on the occupant kinematics, forces on the occupant, and injury patterns and severities for each case.
Respect to the impact direction, the seating orientations could be classified as the frontal/oblique facing (within 0— ± 60 degree orientations or 10, 11, 12, 01, 02 O’clock (OC)), side facing (within ±90— ± 120 or 03, 04, 08, 09 OC), and rear-facing (within ±120–180 degrees or 05, 06, 07 OC). Figure 3 shows the maximum human body movement of each case varying with seat orientations. Significant kinematics differences of the human occupant among the seat facing classifications were observed.
The seat facing classifications and the 50th%ile occupant kinematics under the 40 km/h frontal crash pulse.
Figure 4 (left graph) shows the time-history traces of the head, T1, and pelvis of the frontal/oblique facing seated occupant during the crash. Figure 4 (right graph) depicts the maximum external forces on the occupant from the seatbelt and the seat back. As the occupant faced more obliquely, the Head/T1 displacements increased while the pelvis displacement sightly decreased. The seatbelt routing obviously affected the kinematics. It was observed that the occupant at 11 & 10 OC had larger displacement than 01 & 02 OC. The seatbelt shoulder forces were all above 5 KN, while the seat back force to the occupant increased as the occupant had more side facing.
The 50th%ile occupant kinematics (left graph) and maximum forces on the occupant (right graph) at the frontal/oblique facing seating positions under the 40 km/h frontal crash pulse.
Figure 5 (left graph) shows the time-history traces of the head, T1, and pelvis of the side facing seated occupant during the crash. Figure 5 (right graph) depicts the external forces on the occupant from the seatbelt and the seat back. The occupant at 03 & 04 OC showed twisting head while the torso was restrained by the seat belt and the seat back. The occupant seating at 09 & 08 OC showed shoulder belt slip-off and significantly larger displacement than 03 & 04 OC. In these side facing seat positions, the seatbelt restraint forces were reduced to 2–3 KN, while the seat back forces on the occupant increased to 7.1–8.7 KN.
The 50th%ile occupant kinematics (left graph) and maximum forces on the occupant (right graph) at the side facing seating positions under the 40 km/h frontal crash pulse.
Figure 6 (left graph) shows the time-history traces of the head, T1, and pelvis of the rear facing seated occupant during the crash. Figure 6 (right graph) depicts the maximum seatbelt shoulder forces and the seat back forces on the occupant. No significant difference between 05 OC and far-side 07 OC was shown. In this seat facing group, much larger head and T1 displacement occurred compared to the other two groups. The restraint forces from the seat back increased significantly to 15.5–22.7 KN, while the seatbelt forces were below 1 KN. Hyperextension of the neck was observed.
The 50th%ile occupant kinematics (left graph) and maximum forces on the occupant (right graph) at the rear facing seating positions under the 40 km/h frontal crash pulse.
For each case, the body injury measures, HIC, BrIC, Chest Deflection and Femur Load, were calculated. Figure 7 plots these normalized injury measures varying with the seating orientations. From the HIC and BrIC plots, we see that the more rearward the occupant faced, the larger HIC and BrIC had. The occupant at the front/oblique facing (12–02 OC) showed largest anterior-posterior chest deflection, followed by pure rear facing (06 OC) due to the restraints from the seatbelt or seat back. The occupant at the side facing (04 & 08 OC) showed largest lateral chest deflection, followed by front/oblique facing (11 & 10 OC) because the torso moved laterally to the seat and contacted the seat side structure.
The 50th%ile occupant body region injury measures at all the seating positions under the 40 km/h frontal crash pulse.
Figures 3–6 show that the occupant had the largest torso excursion laterally in the −90 degrees (or 09 OC side-facing) orientated seating position. The maximum Y-displacement of the T1 kinematics target reached 751 mm. This trend was same as what Kitagawa, Y., et al. found in their study similar to this setup [81].
Figures 3–6 show that the shoulder seatbelt had the largest restraint force on the occupant at the 12 OC seating position under the frontal loading, while the restraint force on the occupant from the seat back reached the maximum at the 06 OC seating position.
From Figure 7, the worst cases were identified as
side facing (04 OC) having the highest risks of combination of the head and chest injuries indicated with the largest BrIC and lateral chest deflection, and
rear facing (06 OC) having the highest risks of head and neck injuries due to neck hyperextension.
The results in Section 3 show that a side facing seated occupant could have high risk of head and chest injuries even at a moderate severity frontal crash. Our other previous study [84] concluded that as a frontal crash severity increased above 40kph or 25mph delta velocity, the estimated injury risks for the body regions of head, chest, abdomen, pelvis, and knee-thigh-hip of the side-facing seated occupant increased significantly.
In real-world vehicle crashes, a lateral-facing seated occupant could also be exposed to various impacts other than a frontal crash, such as the oblique, side, and rear vehicle crashes. In this study, we investigated a mid-size male occupant on a 2nd row side-facing seat in a minivan subject to various crash pulses from the current US regulatory vehicle crash tests. The objective was to better understand the body injury risks and restraint protection effectiveness for such a side-facing seated occupant.
The general approach went through the three phases: 1) selected the vehicle crash test cases, collected the test data, and performed the vehicle crash test simulations; 2) performed the occupant simulations and injury analysis; 3) developed new restraint concepts for the occupant protection (the methods and results from this phase will be summarized in Section 5).
In this study, the case vehicle was a US minivan with redesigned seating arrangement for a conceptual automated vehicle.
Eight US regulatory vehicle crash tests for the minivan were considered, as listed in Table 3, including the US NCAP rigid barrier frontal crash (FC-RB), the IIHS 40% offset deformable barrier frontal crash (FC-ODB), the IIHS small overlap rigid barrier frontal crash (FC-SOB), the US NCAP moving deformable barrier near side crash (NS-DB), the IIHS moving deformable high barrier near side crash (NS-IDB), the US NCAP moving deformable barrier far side crash (FS-DB), the IIHS moving deformable high barrier far side crash (FS-IDB), and the NHTSA rear crash sled test (RC-RL).
Case Ref. Name | Crash Test Description | Crash Type | Crash Mode | Delta Velocity | Ref. Test # |
---|---|---|---|---|---|
FC-RB | Frontal Crash, US NCAP Rigid Barrier | Frontal | NCAP Barrier | 56 kph | [85] |
FC-ODB | Frontal Crash, IIHS 40% Offset Deformable Barrier | Frontal oblique | IIHS ODB | 64 kph | [CEF0806] |
FC-SOB | Frontal Crash, IIHS Small Overlap Rigid Barrier | Near side | IIHS SORB | 64 kph | [CEN1438] |
NS-DB | Near Side Crash, US NCAP Moving Deformable Barrier | Near side | NCAP MDB | 61.6 kph | [86] |
NS-IDB | Near Side Crash, IIHS Moving Deformable High Barrier | Near side | IIHS High MDB | 50 kph | [CES0813] |
FS-DB | Far Side Crash, NCAP Moving Deformable Barrier | Far side | NCAP MDB | 61.6 kph | [87] |
FS-IDB | Far Side Crash, IIHS Moving Deformable High Barrier | Far side | IIHS High MDB | 50 kph | [CES0813] |
RC-RL | Rear Crash, Rear Sled test | Rear | Rear Sled | 40 kph | [88] |
The US regulatory vehicle crash tests for the minivan investigated in this study.
The vehicle side crash tests listed in Table 3 were simulated. The vehicle FE model was originally obtained from the public resource hosted by George Washington University National Crash Analysis Center (NCAC). Further updates were made on the side door structures of the minivan model. Correlation of the maximum side door structure deformation against the measured data were achieved. The updated vehicle FE model consisted of 572,555 elements, 604,821 nodes and 694 parts. Figure 8 shows the vehicle crash simulation model setup for the four side crash tests, in which coupled vehicle crash and occupant simulations were performed.
Simulation models for the four US regulatory vehicle side crash tests.
For simulations of the vehicle frontal, oblique and rear crash tests listed in Table 3, a simplified vehicle FE model with 148,437 elements, 153,155 nodes and 47 parts was developed from the original NCAC model. The vehicle crash pulses from the frontal and oblique tests were collected and applied to the vehicle model, as shown in Figure 9.
The vehicle frontal and oblique crash pulses from the four US regulatory vehicle crash tests used for the occupant simulations in this study.
For the occupant simulations, the GHBMC M50-OS v1.8.4 model (updated internally) was used to represent a 50th%ile male occupant. Figure 10 shows the occupant model setup with the interior seating configuration of the minivan. The occupant restrained with a 3-point seatbelt was placed on a concept bench seat (case seat) on the frontal right side in the middle of the vehicle, surrounded by a 1st row right hand side (RHS) seat on his right, a 2nd row rear-facing seat on his front, and the rear-seat on his left.
The crash cases and interior seating configuration of a conceptual automated minivan investigated in this study.
The case seat model consisted of the cushion, seat pan and seatback. The material models of the cushion foam and the cover fabric were carried over from the validated mechanical properties of a passenger seat. The 1st row RHS seat was represented by a validated production passenger seat FE model as a surrogate.
The occupant seating under gravity was simulated initially. Each simulation run through 150 msec of termination time. The final occupant seating position and posture were then defined along with the seat cushion and seatback geometry profiles from the seating simulation at the time when the occupant achieved his equilibrium seating position.
For each of all the US regulatory vehicle crash tests listed in Table 3, the vehicle and occupant simulations were conducted. From the occupant simulation results, we analyzed the occupant kinematic and kinetic response, as well as the injury measures and risks estimated from the injury risk functions summarized in Table 2.
Figure 11 compares the kinematics snapshots at 115 msec of the 50th%ile male occupant at the side facing seat responding to the US NCAP rigid barrier frontal crash (FC-RB), the IIHS 40% offset deformable barrier (FC-ODB) frontal crash, the IIHS small overlap rigid barrier frontal crash (FC-SOB), and the rear impact (RC-RL), respectively. In all the three frontal and oblique crashes, the occupant impacted to the 1st row seat back on his right, while in the rear impact he moved laterally to his left.
The kinematics snapshots at 115 msec of the 50th%ile male occupant at the side facing seat under various vehicle frontal and rear crashes—FC-RB (upper left), FC-ODB (lower right), FC-IDB (upper right), and RC-RL (lower right).
Figure 12 compares the kinematics of the side-facing seated 50th%ile male occupant at 150 msec responding to the US NCAP moving deformable barrier near side crash (NS-DB), the IIHS moving deformable high barrier near side crash (NS-IDB), the US NCAP moving deformable barrier far side crash (FS-DB), and the IIHS moving deformable high barrier far side crash (FS-IDB), respectively. Under the near side crashes, the occupant firstly moved back toward the seatback during about 80 msec and then bounced forward driven by the seatback force. Under the farside crashes, the occupant moved forward all the way from the beginning. His lower legs impacted the side of the 2nd row LHS seat that was pushed toward the occupant by the deforming LHS side door structures of the vehicle.
The kinematics snapshots at 150 msec of the 50th%ile male occupant at the side facing seat under various vehicle side crashes—NS-DB (upper left), NS-IDB (lower right), FS-DB (upper right), and FS-IDB (lower right).
Table 4 summarizes the injury measures for the body regions of head, neck, Thorax, abdomen, pelvis, and lower extremities, outputted from the belted GHBMC M50-OS v1.8.4 (modified) model for the eight crash cases.
Injury | Injury Measure | 1-FCRB | 2-FCOD | 3-FCSOB | 4-NSDB | 5-FSDB | 6-RCRL | 7-NSIDB | 8-FSIDB |
---|---|---|---|---|---|---|---|---|---|
Head AIS3+ (Side) | HIC36 | 1977.6 | 1673.4 | 519.2 | 116.3 | 95.7 | 121.4 | 159.6 | 150 |
Head AIS3+ (Front) | HIC15 | 1483.1 | 1493.2 | 578.4 | 7.4 | 95.7 | 100.3 | 103.2 | 140.1 |
Brain injury | BrIC | 1.3 | 1.34 | 0.89 | 0.53 | 0.39 | 0.55 | 0.46 | 0.45 |
Neck AIS 2+ | IV-INC | 1.87 | 1.9 | 1.85 | 1.12 | 1.2 | 1.82 | 1.39 | 1.8 |
Chest AIS3+ (Front) | Chest Dmax | 55.9 | 55.3 | 30.7 | 30.1 | 46.6 | 57.1 | 36.6 | 47.3 |
Chest AIS3+ (Side) | Chest Half Dmax | 96.3 | 80.5 | 56.3 | 31.5 | 64.5 | 65.4 | 32.2 | 64.8 |
Abdomen AIS3+ | Vmax*Cmax | 1.174 | 1.917 | 2.287 | 0.509 | 2.698 | 0.615 | 0.875 | 1.44 |
Pelvis AIS2+ (Side) | Pubic Force | 3.585 | 4.807 | 2.751 | 0.555 | 0.737 | 1.098 | 0.881 | 0.593 |
KTH AIS2+ (Front) | Femur Force | 4.974 | 4.547 | 3.334 | 2.055 | 5.42 | 3.39 | 1.895 | 5.107 |
Tibial Plateau/Condyle fracture AIS2+ | Tibia Upp Fz | 5.18 | 5.423 | 2.598 | 3.324 | 7.957 | 1.396 | 2.38 | 9.263 |
Tibia/Fibula shaft fracture AIS2+ | Tibia Index RTI | 0.24 | 0.184 | 0.179 | 0.325 | 0.749 | 0.082 | 0.248 | 0.862 |
Calcaneus, Talus, Ankle and Midfoot fracture AIS2+ | Tibia lower Fz | 3.94 | 1.321 | 2.005 | 1.076 | 1.932 | 0.366 | 0.978 | 1.358 |
The injury measures for the body regions of head, neck, thorax, abdomen, pelvis, and lower extremities from the GHBMC M50-OS v1.8.4 (modified) model restrained with the 3 pt. seatbelt for the eight crash cases.
With the body injury risk functions listed Table 2, we calculated the body region injury risks and the Full Body Injury Index FBII of the 50th%ile mid-size male occupant for each crash case.
Figure 13 (Left plot) compares all the injury risks of the head (P_head), chest (P_chest), abdomen (P_abd), pelvis (P_pelvis), tibial (P_tibial), ankle (P_ankle) among the eight crash cases. It shows that the chest injury risks were relatively high across all the cases. Higher head and pelvis injury risks were observed at all the frontal crash cases. Higher lower extremity injury risks were seen at the far side crash cases.
(left plot): The 50th%ile male occupant body region injury risks of the head (P_head), chest (P_chest), abdomen (P_abd), pelvis (P_pelvis), tibial (P_tibial), ankle (P_ankle), and (right plot): The full body injury index FBII among the eight crash cases.
Figure 13 (Right plot) compares the Full Body Injury Index FBII among the eight crash cases. It is indicated that the US NCAP rigid barrier frontal crash (FCRB) caused the highest FBII value while the US NCAP moving deformable barrier near side crash (NS-DB) had the lowest FBII value.
Table 5 summarizes the estimated vulnerable body regions and injury severity for the side-facing seated 50th%ile male occupant responding to the frontal/oblique, rear, near side and farside side crashes, respectively. It is noted that the impacts to the occupant were completely different from the forward-facing seated due to the side-facing seat orientation. The occupant experienced the side impacts from the frontal and oblique vehicle crashes and the frontal impacts from the farside crashes. Severe body injuries for the side-facing occupant were caused the most by the frontal and oblique crashes, followed by the farside crashes, rear crashes, and near-side crashes.
Vehicle Crash | Impact to Occupant | Vulnerable Body Region | Injury Severity |
---|---|---|---|
Frontal & Frontal Oblique Crashes | Side from Right | Head, Neck, Chest, Pelvis, Lower Extremity | Very High |
Far Side Crashes | Frontal | Head, Chest, Lower Extremity | High |
Rear Crashes | Side from Left | Neck, Chest | Moderate |
Near Side Crashes | Rear | Chest | Low |
The estimated vulnerable body regions and injury severity for the side-facing seated 50th%ile male occupant responding to various vehicle crashes.
The severe body injuries for the side-facing seated occupant restrained with 3-point seatbelt from the frontal, oblique and rear crashes indicated ineffectiveness of the seatbelt restraint for such crash scenarios.
For the farside crashes, the seatbelt performed better for the frontal impacted experienced occupant. The high injury risk value of the lower extremity was caused by contact of the legs to the 2nd row seat.
The near-side crashes caused less severe injuries to the rear impacted experienced occupant possibly due to mitigation of the impact energy by the seat back and the vehicle side structures.
The estimated outcomes of the body injury risks were limited to one case vehicle interior configuration. Further investigation on different vehicle crashes and seating configurations should be performed.
To protect the side-facing seated occupant better, we developed new restraint concepts and evaluated the effectiveness based on understanding of the results from the phase 1–2 presented in Section 4.
First of all, design guidelines for new restraint devices were defined specifically for the side-facing occupant. The requirements for the restraints’ performances are such that: 1) the pelvis lateral movement should be restrained earlier and properly; 2) the head/torso lateral displacements should be minimized to prevent the head/torso contact to any laterally nearby objects; 3) the lower legs/foot lateral failing motion and impact to the 2nd row LHS seat should be minimized.
Four new restraint concept designs highlighted below were developed:
Seat-mounted Side Airbag (SSAB)—integrated to the occupant seat, designed for protection of the occupant from side impacts.
Torso Restrain Airbag (TRAB))—integrated with the lap-seatbelt or to the occupant seat, designed for protection of the occupant from frontal and oblique impacts.
Seat-mounted Head Airbag (HAB)—mounted on the side door structure, designed for protection of the occupant from rear impacts.
Leg Restraint Device (LRD)—mounted beneath of the floor, designed for control of the lower legs/foot lateral failing motion from high severe side impacts.
Figure 14 shows snapshots of the deployed restraints of the SSAB, TRAB, HAB, and LRD, respective.
The new concepts of restraint devices.
Evaluation of the restraint effectiveness was performed in two steps: 1) new restraint concept evaluation; 2) integrated restraint system performance evaluation.
The 1st step was development of the new restraint concepts one by one, for which a component model was created. Its system performance was then evaluated only at one worst vehicle crash test case. For each protection type, the restraint system integration and performance were optimized. The best performed integrated restraints were then selected for the next step study. Table 6 shows the new restraint concept evaluation matrix.
Protection Type | Frontal Protection | Side Protection -Right | Side Protection - Left | Rear Protection |
---|---|---|---|---|
Restraint Device | 3 pt. Seatbelt | 3 pt. Seatbelt | 3 pt. Seatbelt | 3 pt. Seatbelt |
Torso Restrain Airbag (TRAB) | Seat-mounted Side Airbag (SSAB) | Seat-mounted Side Airbag (SSAB) | Seat-mounted Head Airbag (HAB) | |
Leg Restraint Device (LRD | Leg Restraint Device (LRD) | |||
Test Case for Evaluation | FS-DB | FC-RB | RR-SL | NS-DB |
CAE Cases | 12 | 32 | 12 | 8 |
New restraint concept evaluation matrix.
The 2nd step was to verify the system performance of the integrated restraints across all the eight crashes in Table 3. Table 7 shows the evaluation matrix for the three integrated restraint systems—the baseline 3 pt. seatbelt from Section 4, a 4 pt. seatbelt and the “optimal” new restraint system from Step 1 of current study.
Baseline | 4 pt. Seatbelt (SB) | New Constraints | |
---|---|---|---|
Restraint Device | 3 pt. Seatbelt (Baseline) | 4 pt. Seatbelt | 3 pt. Seatbelt |
SSAB, TRAB, LRD,HAB | |||
Crash Cases for Evaluation | FC-RB | FC-RB | FC-RB |
FC-ODB | FC-ODB | FC-ODB | |
FC-SOB | FC-SOB | FC-SOB | |
NS-DB | NS-DB | NS-DB | |
NS-IDB | NS-IDB | NS-IDB | |
FS-DB | FS-DB | FS-DB | |
FS-IDB | FS-IDB | FS-IDB | |
RC-RL | RC-RL | RC-RL | |
CAE Cases | 8 | 8 | 8 |
Integrated restraint system performance evaluation matrix.
Figure 15 compares the kinematics snapshots at 120 msec of the side-facing seated 50th%ile male occupant with the three restraint systems under the US NCAP rigid barrier frontal crash (FC-RB) (worst case). With the new restraint system, the occupant was protected from being impacted from the 1st row seat on his right side, while the occupant with the other two restraints (3 pt. and 4 pt. seatbelt) impacted heavily to the 1st row right seat on his right.
The kinematics snapshots at 120 msec of the side-facing seated 50th%ile male occupant under the US NCAP rigid barrier frontal crash (FC-RB) with the three restraint systems—3 pt. SB (left), 4 pt. SB (middle), and new restraints (right).
Table 8 summarizes the injury measures for the body regions of head, neck, Thorax, abdomen, pelvis, and lower extremities, outputted from the GHBMC M50-OS v1.8.4 (modified) model restrained with the new restraints for the eight crash cases.
Injury | Injury Measure | 17-FCRB_NEWRS | 18-FCODB_NEWRS | 19-FCSOB_NEWRS | 20-NSDB_NEWRS | 21-FSDB_NEWRS | 22-RCRL_NEWRS | 23-NSIDB_NEWRS | 24-FSIDB_NEWRS |
---|---|---|---|---|---|---|---|---|---|
Head AIS3+ (Side) | HIC36 | 250.5 | 204.5 | 150 | 113.3 | 117.4 | 76.1 | 150.1 | 104.1 |
Head AIS3+ (Fronta) | HIC15 | 174.4 | 132.9 | 150 | 75.7 | 93.6 | 65.9 | 91.9 | 58.6 |
Brain injury AIS 4+ | BrIC | 0.81 | 0.76 | 0.83 | 0.52 | 0.52 | 0.33 | 0.49 | 0.59 |
Neck AIS 2+ | IV-INC | 1.11 | 1.22 | 1.5 | 1.79 | 1.52 | 1.52 | 1.43 | 1.3 |
Chest AIS3+ (Front) | Chest Dmax | 35.6 | 38.4 | 28.3 | 23.1 | 34.4 | 17.4 | 32.1 | 43.1 |
Chest AIS3+ (Side) | ChestHalf Dmax | 56.3 | 58.0 | 34.9 | 29.2 | 44.8 | 25.1 | 25.2 | 47.9 |
Abdomen AIS 2+ | Vmax*Cmax | 0.623 | 0.615 | 0.381 | 0.288 | 1.529 | 0.125 | 0.877 | 1.313 |
Pelvis AIS2 + -(side) | Pubic Force | 2.935 | 1.423 | 2.109 | 0.666 | 0.743 | 0.560 | 1.004 | 0.951 |
KTH AIS2+ (front) | Femur Force | 3.548 | 4.704 | 3.310 | 2.019 | 5.933 | 1.856 | 2.160 | 4.476 |
Tibial Plateau/Condyle fracture AIS2+ | Tibia Upp Fz | 3.584 | 2.740 | 3.837 | 2.642 | 4.721 | 1.567 | 1.891 | 4.731 |
Tibia/Fibula shaft fracture AIS2+ | Tibia Index RTI | 0.413 | 0.443 | 0.281 | 0.124 | 0.950 | 0.232 | 0.158 | 0.622 |
Calcaneus, Talus, Ankle & Midfoot fracture AIS 2+ | Tibia lower Fz | 1.293 | 0.733 | 2.195 | 1.029 | 1.125 | 0.467 | 1.127 | 1.350 |
The injury measures for the body regions of the side-facing seated 50th%ile occupant restrained with the new restraints for the eight crash cases.
Figure 16 compares the body injury risks of the side-facing seated 50th%ile male occupant for the vehicle frontal & rear crash cases, restrained with 1) baseline 3 pt. SB (in blue), 2) 4 ps SB (in Orange), and 3) new restraints. We see that the new restraint system significantly reduced all the body region risks compared to the 3 pt. SB restraint system.
Comparison of the body injury risks of the side-facing seated 50th%ile male occupant for the vehicle frontal & rear crash cases, restrained with baseline 3 pt. SB (blue), 4 pt. SB (Orange), and new restraints (green).
Figure 17 compares the body injury risks of the side-facing seated 50th%ile male occupant for the vehicle side crash cases, restrained with 1) baseline 3 pt. SB (in blue), 2) 4 ps SB (in Orange), and 3) new restraints. It showed that under all the side crash conditions the new restraint system also worked effectively for reducing the severe injury risks compared to the 3 pt. SB restraint baseline.
Comparison of the side-facing seated 50th%ile male occupant body injury risks for the vehicle near side and farside crash cases, restrained with baseline 3 pt. SB (blue), 4 pt. SB (Orange), and new restraints (green).
Figure 18 compares the Full Body Injury Index of the side-facing seated 50th%ile male occupant with three restraint systems from all the vehicle crash cases. Overall, the new restraint system significantly reduced the risks from all the vehicle crash tests in Table 3 compared to the other evaluated seatbelt only restraints.
Comparison of the full body injury index of the side-facing seated 50th%ile male occupant across all the vehicle crash cases, restrained with baseline 3 pt. SB (blue), 4 pt. SB (Orange), and new restraints (green).
This study indicated that the conventional seatbelt system (with baseline 3-pt seatbelt alone) did not provide sufficient protection for the side-facing seated occupant. The same conclusion was also obtained from our other study on both 50th%ile male and 5th%ile female human occupants in a side-facing seat [84].
The 4-pt seatbelt restrain system investigated from this study did not show good performance. Further work was needed to improve the 4-pt restraint design and the restraint component model validation.
The new restraints concepts developed in this study were shown to be capable of effectively protecting the far-side seating occupant at different vehicle crash conditions. The restraint system consisted of the three restraint components, among which the seat-mounted side airbag (SSAB) was a key component that protected the head/neck and torso more effectively. To further develop this concept design into a product in mass protection, more future work is required to resolve possible issues in the packaging and the manufacturing.
Among different seating orientations of 360 degrees respect to the impact direction under the 40 kph frontal crash pulse, the side-facing positions were identified as worst cases in which the occupant had the highest risks of combination of the head and chest injuries indicated with the largest BrIC and lateral chest deflection, while the rear facing seated occupant had the highest risk of cervical spinal neck injury due to the neck hyperextension.
For the US regulatory (NCAP and IIHS) vehicle frontal and oblique crash tests (including NCAP rigid barrier frontal crash, the IIHS 40% offset deformable barrier frontal crash, and the IIHS small overlap rigid barrier frontal crash), as well as the vehicle rear crash test, side protection of a side-facing seated occupant is required. As the crash severities increased to 65kph or 35 mph of delta velocity, the side-facing occupant with the 3 pt. seatbelt alone could suffer high injury risks for the multiple body regions of head, chest, abdomen, pelvis, and the lower extremities.
Under the US regulatory (NCAP and IIHS) vehicle far side crash tests (including the US NCAP moving deformable barrier far side crash and the IIHS moving deformable high barrier far side crash), frontal protection for a side-facing seated occupant restrained with a 3 pt. seatbelt is necessary. Such an occupant could suffer moderate to high injury risks for the head, chest, and the lower extremities.
Under the US regulatory (NCAP and IIHS) vehicle near side crash tests (including the US NCAP moving deformable barrier near side crash and the IIHS moving deformable high barrier near side crash), a side-facing seated occupant will experience the rear impact under large pushing force from the seat due to the side door structure intrusion. With the seat and 3 pt. seatbelt restrains, such an occupant could suffer moderate injury risks for the head, neck and chest.
The new restraint concepts developed for the side-facing seat occupant in Section 5 demonstrated significant improvement for mitigation of the occupant’s body injuries for all the vehicle crash test conditions considered in this study.
We acknowledge Sungwoo Lee and Maika Katagiri who helped analyzing the occupant injury analysis data and Parred Kumar Jakkamsetti who helped modeling and analyzing of the restraint concept models in this research.
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Thin films are considered as backbone for advanced applications in the various fields such as optical devices, environmental applications, telecommunications devices, energy storage devices, and so on . The crucial issue for all applications of thin films depends on their morphology and the stability. The morphology of the thin films strongly hinges on deposition techniques. Thin films can be deposited by the physical and chemical routes. In this chapter, we discuss some advance techniques and principles of thin-film depositions. The vacuum thermal evaporation technique, electron beam evaporation, pulsed-layer deposition, direct current/radio frequency magnetron sputtering, and chemical route deposition systems will be discussed in detail.",book:{id:"5541",slug:"modern-technologies-for-creating-the-thin-film-systems-and-coatings",title:"Modern Technologies for Creating the Thin-film Systems and Coatings",fullTitle:"Modern Technologies for Creating the Thin-film Systems and Coatings"},signatures:"Asim Jilani, Mohamed Shaaban Abdel-wahab and Ahmed Hosny\nHammad",authors:[{id:"192377",title:"Dr.",name:"Asim",middleName:null,surname:"Jilani",slug:"asim-jilani",fullName:"Asim Jilani"},{id:"192972",title:"Dr.",name:"M.Sh",middleName:null,surname:"Abdel-Wahab",slug:"m.sh-abdel-wahab",fullName:"M.Sh Abdel-Wahab"},{id:"192973",title:"Dr.",name:"Ahmed",middleName:"H",surname:"Hammad",slug:"ahmed-hammad",fullName:"Ahmed Hammad"}]},{id:"17722",doi:"10.5772/23174",title:"Study of SiO2/Si Interface by Surface Techniques",slug:"study-of-sio2-si-interface-by-surface-techniques",totalDownloads:14143,totalCrossrefCites:13,totalDimensionsCites:35,abstract:null,book:{id:"332",slug:"crystalline-silicon-properties-and-uses",title:"Crystalline Silicon",fullTitle:"Crystalline Silicon - Properties and Uses"},signatures:"Rodica Ghita, Constantin Logofatu, Catalin-Constantin Negrila, Florica Ungureanu, Costel Cotirlan, Adrian-Stefan Manea, Mihail-Florin Lazarescu and Corneliu Ghica",authors:[{id:"50919",title:"Dr.",name:"Rodica V.",middleName:null,surname:"Ghita",slug:"rodica-v.-ghita",fullName:"Rodica V. 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The principles underlying RF‐magnetron sputtering used to prepare calcium phosphate‐based, mainly hydroxyapatite coatings, are discussed in this chapter. The fundamental characteristic of the RF‐magnetron sputtering is an energy input into the growing film. In order to tailor the film properties, one has to adjust the energy input into the substrate depending on the desired film properties. The effect of different deposition control parameters, such as deposition time, substrate temperature, and substrate biasing on the hydroxyapatite (HA) film properties is discussed.",book:{id:"5541",slug:"modern-technologies-for-creating-the-thin-film-systems-and-coatings",title:"Modern Technologies for Creating the Thin-film Systems and Coatings",fullTitle:"Modern Technologies for Creating the Thin-film Systems and Coatings"},signatures:"Roman Surmenev, Alina Vladescu, Maria Surmeneva, Anna Ivanova,\nMariana Braic, Irina Grubova and Cosmin Mihai Cotrut",authors:[{id:"193921",title:"Dr.",name:"Alina",middleName:null,surname:"Vladescu",slug:"alina-vladescu",fullName:"Alina Vladescu"},{id:"193922",title:"Prof.",name:"Roman",middleName:null,surname:"Surmenev",slug:"roman-surmenev",fullName:"Roman Surmenev"},{id:"193923",title:"Dr.",name:"Maria",middleName:null,surname:"Surmeneva",slug:"maria-surmeneva",fullName:"Maria Surmeneva"},{id:"193948",title:"Dr.",name:"Mariana",middleName:null,surname:"Braic",slug:"mariana-braic",fullName:"Mariana Braic"},{id:"194047",title:"Ms.",name:"Anna",middleName:null,surname:"Ivanova",slug:"anna-ivanova",fullName:"Anna Ivanova"},{id:"194048",title:"BSc.",name:"Irina",middleName:null,surname:"Grubova",slug:"irina-grubova",fullName:"Irina Grubova"},{id:"196398",title:"Prof.",name:"Cosmin Mihai",middleName:null,surname:"Cotrut",slug:"cosmin-mihai-cotrut",fullName:"Cosmin Mihai Cotrut"}]},{id:"21157",doi:"10.5772/24330",title:"Compilation on Synthesis, Characterization and Properties of Silicon and Boron Carbonitride Films",slug:"compilation-on-synthesis-characterization-and-properties-of-silicon-and-boron-carbonitride-films",totalDownloads:5200,totalCrossrefCites:6,totalDimensionsCites:19,abstract:null,book:{id:"326",slug:"silicon-carbide-materials-processing-and-applications-in-electronic-devices",title:"Silicon Carbide",fullTitle:"Silicon Carbide - Materials, Processing and Applications in Electronic Devices"},signatures:"P. Hoffmann, N. Fainer, M. Kosinova, O. Baake and W. Ensinger",authors:[{id:"56722",title:"Dr.",name:"Peter",middleName:null,surname:"Hoffmann",slug:"peter-hoffmann",fullName:"Peter Hoffmann"},{id:"56726",title:"Dr.",name:"Marina",middleName:null,surname:"Kosinova",slug:"marina-kosinova",fullName:"Marina Kosinova"},{id:"56727",title:"Prof.",name:"Wolfgang",middleName:null,surname:"Ensinger",slug:"wolfgang-ensinger",fullName:"Wolfgang Ensinger"}]}],mostDownloadedChaptersLast30Days:[{id:"52684",title:"Advance Deposition Techniques for Thin Film and Coating",slug:"advance-deposition-techniques-for-thin-film-and-coating",totalDownloads:7639,totalCrossrefCites:32,totalDimensionsCites:59,abstract:"Thin films have a great impact on the modern era of technology. Thin films are considered as backbone for advanced applications in the various fields such as optical devices, environmental applications, telecommunications devices, energy storage devices, and so on . The crucial issue for all applications of thin films depends on their morphology and the stability. The morphology of the thin films strongly hinges on deposition techniques. Thin films can be deposited by the physical and chemical routes. In this chapter, we discuss some advance techniques and principles of thin-film depositions. The vacuum thermal evaporation technique, electron beam evaporation, pulsed-layer deposition, direct current/radio frequency magnetron sputtering, and chemical route deposition systems will be discussed in detail.",book:{id:"5541",slug:"modern-technologies-for-creating-the-thin-film-systems-and-coatings",title:"Modern Technologies for Creating the Thin-film Systems and Coatings",fullTitle:"Modern Technologies for Creating the Thin-film Systems and Coatings"},signatures:"Asim Jilani, Mohamed Shaaban Abdel-wahab and Ahmed Hosny\nHammad",authors:[{id:"192377",title:"Dr.",name:"Asim",middleName:null,surname:"Jilani",slug:"asim-jilani",fullName:"Asim Jilani"},{id:"192972",title:"Dr.",name:"M.Sh",middleName:null,surname:"Abdel-Wahab",slug:"m.sh-abdel-wahab",fullName:"M.Sh Abdel-Wahab"},{id:"192973",title:"Dr.",name:"Ahmed",middleName:"H",surname:"Hammad",slug:"ahmed-hammad",fullName:"Ahmed Hammad"}]},{id:"68467",title:"Semiconductor Nanocomposites for Visible Light Photocatalysis of Water Pollutants",slug:"semiconductor-nanocomposites-for-visible-light-photocatalysis-of-water-pollutants",totalDownloads:1803,totalCrossrefCites:7,totalDimensionsCites:11,abstract:"Semiconductor photocatalysis gained reputation in the early 1970s when Fujishima and Honda revealed the potential of TiO2 to split water in to hydrogen and oxygen in a photoelectrochemical cell. Their work provided the base for the development of semiconductor photocatalysis for the environmental remediation and energy applications. Photoactivity of some semiconductors was found to be low due to larger band gap energy and higher electron-hole pair recombination rate. To avoid these problems, the development of visible light responsive photocatalytic materials by different approaches, such as metal and/or non-metal doping, co-doping, coupling of semiconductors, composites and heterojunctions materials synthesis has been widely investigated and explored in systematic manner. This chapter emphasizes on the different type of tailored photocatalyst materials having the enhanced visible light absorption properties, lower band gap energy and recombination rate of electron-hole pairs and production of reactive radical species. Visible light active semiconductors for the environmental remediation purposes, particularly for water treatment and disinfection are also discussed in detail. Studies on the photocatalytic degradation of emerging organic compounds like cyanotoxins, VOCs, phenols, pharmaceuticals, etc., by employing variety of modified semiconductors, are summarized, and a mechanistic aspects of the photocatalysis has been discussed.",book:{id:"7671",slug:"concepts-of-semiconductor-photocatalysis",title:"Concepts of Semiconductor Photocatalysis",fullTitle:"Concepts of Semiconductor Photocatalysis"},signatures:"Fatima Imtiaz, Jamshaid Rashid and Ming Xu",authors:[{id:"292882",title:"Dr.",name:"Jamshaid",middleName:null,surname:"Rashid",slug:"jamshaid-rashid",fullName:"Jamshaid Rashid"},{id:"302498",title:"Ms.",name:"Fatima",middleName:null,surname:"Imtiaz",slug:"fatima-imtiaz",fullName:"Fatima Imtiaz"},{id:"308434",title:"Prof.",name:"Ming",middleName:null,surname:"Xu",slug:"ming-xu",fullName:"Ming Xu"}]},{id:"17728",title:"Defect Related Luminescence in Silicon Dioxide Network: A Review",slug:"defect-related-luminescence-in-silicon-dioxide-network-a-review",totalDownloads:9472,totalCrossrefCites:46,totalDimensionsCites:98,abstract:null,book:{id:"332",slug:"crystalline-silicon-properties-and-uses",title:"Crystalline Silicon",fullTitle:"Crystalline Silicon - Properties and Uses"},signatures:"Roushdey Salh",authors:[{id:"48391",title:"Dr.",name:"Roushdey",middleName:null,surname:"Salh",slug:"roushdey-salh",fullName:"Roushdey Salh"}]},{id:"58469",title:"The Electrochemical Performance of Deposited Manganese Oxide-Based Film as Electrode Material for Electrochemical Capacitor Application",slug:"the-electrochemical-performance-of-deposited-manganese-oxide-based-film-as-electrode-material-for-el",totalDownloads:1736,totalCrossrefCites:4,totalDimensionsCites:8,abstract:"The transition metal oxide has been recognized as one of the promising electrode materials for electrochemical capacitor application. Due to the participation of charge transfer reactions, the capacitance offered by transition metal oxide can be higher compared to double layer capacitance. The investigation on hydrous ruthenium oxide has revealed the surface redox reactions that contributed to the wide potential window shown on cyclic voltammetry curve. Although the performance of ruthenium oxide is impressive, its toxicity has limited itself from commercial application. Manganese oxide is a pseudocapacitive material behaves similar to ruthenium oxide. It consists of various oxidation states which allow the occurrence of redox reactions. It is also environmental friendly, low cost, and natural abundant. The charge storage of manganese oxide film takes into account of the redox reactions between Mn3+ and Mn4+ and can be accounted to two mechanisms. The first one involves the intercalation/deintercalation of electrolyte ions and/or protons upon reduction/oxidation processes. The second contributor for the charge storage is due to the surface adsorption of electrolyte ions on the electrode surface.",book:{id:"6083",slug:"semiconductors-growth-and-characterization",title:"Semiconductors",fullTitle:"Semiconductors - Growth and Characterization"},signatures:"Chan Pei Yi and Siti Rohana Majid",authors:[{id:"197956",title:"Associate Prof.",name:"S.R.",middleName:null,surname:"Majid",slug:"s.r.-majid",fullName:"S.R. Majid"},{id:"216449",title:"Ms.",name:"Pei Yi",middleName:null,surname:"Chan",slug:"pei-yi-chan",fullName:"Pei Yi Chan"}]},{id:"60792",title:"TCAD Device Modelling and Simulation of Wide Bandgap Power Semiconductors",slug:"tcad-device-modelling-and-simulation-of-wide-bandgap-power-semiconductors",totalDownloads:2113,totalCrossrefCites:15,totalDimensionsCites:15,abstract:"Technology computer-aided Design (TCAD) is essential for devices technology development, including wide bandgap power semiconductors. However, most TCAD tools were originally developed for silicon and their performance and accuracy for wide bandgap semiconductors is contentious. This chapter will deal with TCAD device modelling of wide bandgap power semiconductors. In particular, modelling and simulating 3C- and 4H-Silicon Carbide (SiC), Gallium Nitride (GaN) and Diamond devices are examined. The challenges associated with modelling the material and device physics are analyzed in detail. It also includes convergence issues and accuracy of predicted performance. 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Heshmati",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/313921/images/system/313921.jpg",biography:"Dr. Hassan Massoud Heshmati is an endocrinologist with 46 years of experience in clinical research in academia (university-affiliated hospitals, Paris, France; Mayo Foundation, Rochester, MN, USA) and pharmaceutical companies (Sanofi, Malvern, PA, USA; Essentialis, Carlsbad, CA, USA; Gelesis, Boston, MA, USA). His research activity focuses on pituitary tumors, hyperthyroidism, thyroid cancers, osteoporosis, diabetes, and obesity. He has extensive knowledge in the development of anti-obesity products. Dr. Heshmati is the author of 299 abstracts, chapters, and articles related to endocrinology and metabolism. He is currently a consultant at Endocrinology Metabolism Consulting, LLC, Anthem, AZ, USA.",institutionString:"Endocrinology Metabolism Consulting, LLC",institution:null},{id:"76477",title:"Prof.",name:"Mirza",middleName:null,surname:"Hasanuzzaman",slug:"mirza-hasanuzzaman",fullName:"Mirza Hasanuzzaman",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/76477/images/system/76477.png",biography:"Dr. Mirza Hasanuzzaman is a Professor of Agronomy at Sher-e-Bangla Agricultural University, Bangladesh. He received his Ph.D. in Plant Stress Physiology and Antioxidant Metabolism from Ehime University, Japan, with a scholarship from the Japanese Government (MEXT). Later, he completed his postdoctoral research at the Center of Molecular Biosciences, University of the Ryukyus, Japan, as a recipient of the Japan Society for the Promotion of Science (JSPS) postdoctoral fellowship. He was also the recipient of the Australian Government Endeavour Research Fellowship for postdoctoral research as an adjunct senior researcher at the University of Tasmania, Australia. Dr. Hasanuzzaman’s current work is focused on the physiological and molecular mechanisms of environmental stress tolerance. Dr. Hasanuzzaman has published more than 150 articles in peer-reviewed journals. He has edited ten books and written more than forty book chapters on important aspects of plant physiology, plant stress tolerance, and crop production. According to Scopus, Dr. Hasanuzzaman’s publications have received more than 10,500 citations with an h-index of 53. He has been named a Highly Cited Researcher by Clarivate. He is an editor and reviewer for more than fifty peer-reviewed international journals and was a recipient of the “Publons Peer Review Award” in 2017, 2018, and 2019. He has been honored by different authorities for his outstanding performance in various fields like research and education, and he has received the World Academy of Science Young Scientist Award (2014) and the University Grants Commission (UGC) Award 2018. He is a fellow of the Bangladesh Academy of Sciences (BAS) and the Royal Society of Biology.",institutionString:"Sher-e-Bangla Agricultural University",institution:{name:"Sher-e-Bangla Agricultural University",country:{name:"Bangladesh"}}},{id:"187859",title:"Prof.",name:"Kusal",middleName:"K.",surname:"Das",slug:"kusal-das",fullName:"Kusal Das",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSBDeQAO/Profile_Picture_1623411145568",biography:"Kusal K. Das is a Distinguished Chair Professor of Physiology, Shri B. M. Patil Medical College and Director, Centre for Advanced Medical Research (CAMR), BLDE (Deemed to be University), Vijayapur, Karnataka, India. Dr. Das did his M.S. and Ph.D. in Human Physiology from the University of Calcutta, Kolkata. His area of research is focused on understanding of molecular mechanisms of heavy metal activated low oxygen sensing pathways in vascular pathophysiology. He has invented a new method of estimation of serum vitamin E. His expertise in critical experimental protocols on vascular functions in experimental animals was well documented by his quality of publications. He was a Visiting Professor of Medicine at University of Leeds, United Kingdom (2014-2016) and Tulane University, New Orleans, USA (2017). For his immense contribution in medical research Ministry of Science and Technology, Government of India conferred him 'G.P. Chatterjee Memorial Research Prize-2019” and he is also the recipient of 'Dr.Raja Ramanna State Scientist Award 2015” by Government of Karnataka. He is a Fellow of the Royal Society of Biology (FRSB), London and Honorary Fellow of Karnataka Science and Technology Academy, Department of Science and Technology, Government of Karnataka.",institutionString:"BLDE (Deemed to be University), India",institution:null},{id:"243660",title:"Dr.",name:"Mallanagouda Shivanagouda",middleName:null,surname:"Biradar",slug:"mallanagouda-shivanagouda-biradar",fullName:"Mallanagouda Shivanagouda Biradar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/243660/images/system/243660.jpeg",biography:"M. S. Biradar is Vice Chancellor and Professor of Medicine of\nBLDE (Deemed to be University), Vijayapura, Karnataka, India.\nHe obtained his MD with a gold medal in General Medicine and\nhas devoted himself to medical teaching, research, and administrations. He has also immensely contributed to medical research\non vascular medicine, which is reflected by his numerous publications including books and book chapters. Professor Biradar was\nalso Visiting Professor at Tulane University School of Medicine, New Orleans, USA.",institutionString:"BLDE (Deemed to be University)",institution:{name:"BLDE University",country:{name:"India"}}},{id:"289796",title:"Dr.",name:"Swastika",middleName:null,surname:"Das",slug:"swastika-das",fullName:"Swastika Das",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/289796/images/system/289796.jpeg",biography:"Swastika N. Das is Professor of Chemistry at the V. P. Dr. P. G.\nHalakatti College of Engineering and Technology, BLDE (Deemed\nto be University), Vijayapura, Karnataka, India. She obtained an\nMSc, MPhil, and PhD in Chemistry from Sambalpur University,\nOdisha, India. Her areas of research interest are medicinal chemistry, chemical kinetics, and free radical chemistry. She is a member\nof the investigators who invented a new modified method of estimation of serum vitamin E. She has authored numerous publications including book\nchapters and is a mentor of doctoral curriculum at her university.",institutionString:"BLDEA’s V.P.Dr.P.G.Halakatti College of Engineering & Technology",institution:{name:"BLDE University",country:{name:"India"}}},{id:"248459",title:"Dr.",name:"Akikazu",middleName:null,surname:"Takada",slug:"akikazu-takada",fullName:"Akikazu Takada",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/248459/images/system/248459.png",biography:"Akikazu Takada was born in Japan, 1935. After graduation from\nKeio University School of Medicine and finishing his post-graduate studies, he worked at Roswell Park Memorial Institute NY,\nUSA. He then took a professorship at Hamamatsu University\nSchool of Medicine. In thrombosis studies, he found the SK\npotentiator that enhances plasminogen activation by streptokinase. He is very much interested in simultaneous measurements\nof fatty acids, amino acids, and tryptophan degradation products. By using fatty\nacid analyses, he indicated that plasma levels of trans-fatty acids of old men were\nfar higher in the US than Japanese men. . He also showed that eicosapentaenoic acid\n(EPA) and docosahexaenoic acid (DHA) levels are higher, and arachidonic acid\nlevels are lower in Japanese than US people. By using simultaneous LC/MS analyses\nof plasma levels of tryptophan metabolites, he recently found that plasma levels of\nserotonin, kynurenine, or 5-HIAA were higher in patients of mono- and bipolar\ndepression, which are significantly different from observations reported before. In\nview of recent reports that plasma tryptophan metabolites are mainly produced by\nmicrobiota. He is now working on the relationships between microbiota and depression or autism.",institutionString:"Hamamatsu University School of Medicine",institution:{name:"Hamamatsu University School of Medicine",country:{name:"Japan"}}},{id:"137240",title:"Prof.",name:"Mohammed",middleName:null,surname:"Khalid",slug:"mohammed-khalid",fullName:"Mohammed Khalid",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/137240/images/system/137240.png",biography:"Mohammed Khalid received his B.S. in Chemistry in July 2000, and his Ph.D. in Physical Chemistry in 2007 from the University of Khartoum, Sudan. In 2009 he joined the Dr. Ron Clarke research group at the School of Chemistry, Faculty of Science, University of Sydney, Australia as a postdoctoral fellow where he worked on the Interaction of ATP with the phosphoenzyme of the Na+, K+-ATPase, and Dual mechanisms of allosteric acceleration of the Na+, K+-ATPase by ATP. He then worked as Assistant Professor at the Department of Chemistry, University of Khartoum, and in 2014 was promoted to Associate Professor ranking. In 2011 he joined the staff of the Chemistry Department at Taif University, Saudi Arabia, where he is currently active as an Assistant Professor. His research interests include:\r\n(1) P-type ATPase Enzyme Kinetics and Mechanisms; (2) Kinetics and Mechanism of Redox Reactions; (3) Autocatalytic reactions; (4) Computational enzyme kinetics; (5) Allosteric acceleration of P-type ATPases by ATP; (6) Exploring of allosteric sites of ATPases and interaction of ATP with ATPases located in the cell membranes.",institutionString:"Taif University",institution:{name:"Taif University",country:{name:"Saudi Arabia"}}},{id:"63810",title:"Prof.",name:"Jorge",middleName:null,surname:"Morales-Montor",slug:"jorge-morales-montor",fullName:"Jorge Morales-Montor",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/63810/images/system/63810.png",biography:"Dr. Jorge Morales-Montor was recognized with the Lola and Igo Flisser PUIS Award for best graduate thesis at the national level in the field of parasitology. He received a fellowship from the Fogarty Foundation to perform postdoctoral research stay at the University of Georgia. He has 153 journal articles to his credit. He has also edited several books and published more than fifty-five book chapters. He is a member of the Mexican Academy of Sciences, Latin American Academy of Sciences, and the National Academy of Medicine. He has received more than thirty-five awards and has supervised numerous bachelor’s, master’s, and Ph.D. students. Dr. Morales-Montor is the past president of the Mexican Society of Parasitology.",institutionString:"National Autonomous University of Mexico",institution:{name:"National Autonomous University of Mexico",country:{name:"Mexico"}}},{id:"217215",title:"Dr.",name:"Palash",middleName:null,surname:"Mandal",slug:"palash-mandal",fullName:"Palash Mandal",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/217215/images/system/217215.jpeg",biography:null,institutionString:"Charusat University",institution:null},{id:"49739",title:"Dr.",name:"Leszek",middleName:null,surname:"Szablewski",slug:"leszek-szablewski",fullName:"Leszek Szablewski",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/49739/images/system/49739.jpg",biography:"Leszek Szablewski is a professor of medical sciences. He received his M.S. in the Faculty of Biology from the University of Warsaw and his PhD degree from the Institute of Experimental Biology Polish Academy of Sciences. He habilitated in the Medical University of Warsaw, and he obtained his degree of Professor from the President of Poland. Professor Szablewski is the Head of Chair and Department of General Biology and Parasitology, Medical University of Warsaw. Professor Szablewski has published over 80 peer-reviewed papers in journals such as Journal of Alzheimer’s Disease, Biochim. Biophys. Acta Reviews of Cancer, Biol. Chem., J. Biomed. Sci., and Diabetes/Metabol. Res. Rev, Endocrine. He is the author of two books and four book chapters. He has edited four books, written 15 scripts for students, is the ad hoc reviewer of over 30 peer-reviewed journals, and editorial member of peer-reviewed journals. Prof. Szablewski’s research focuses on cell physiology, genetics, and pathophysiology. He works on the damage caused by lack of glucose homeostasis and changes in the expression and/or function of glucose transporters due to various diseases. He has given lectures, seminars, and exercises for students at the Medical University.",institutionString:"Medical University of Warsaw",institution:{name:"Medical University of Warsaw",country:{name:"Poland"}}},{id:"173123",title:"Dr.",name:"Maitham",middleName:null,surname:"Khajah",slug:"maitham-khajah",fullName:"Maitham Khajah",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/173123/images/system/173123.jpeg",biography:"Dr. Maitham A. Khajah received his degree in Pharmacy from Faculty of Pharmacy, Kuwait University, in 2003 and obtained his PhD degree in December 2009 from the University of Calgary, Canada (Gastrointestinal Science and Immunology). Since January 2010 he has been assistant professor in Kuwait University, Faculty of Pharmacy, Department of Pharmacology and Therapeutics. His research interest are molecular targets for the treatment of inflammatory bowel disease (IBD) and the mechanisms responsible for immune cell chemotaxis. He cosupervised many students for the MSc Molecular Biology Program, College of Graduate Studies, Kuwait University. Ever since joining Kuwait University in 2010, he got various grants as PI and Co-I. He was awarded the Best Young Researcher Award by Kuwait University, Research Sector, for the Year 2013–2014. He was a member in the organizing committee for three conferences organized by Kuwait University, Faculty of Pharmacy, as cochair and a member in the scientific committee (the 3rd, 4th, and 5th Kuwait International Pharmacy Conference).",institutionString:"Kuwait University",institution:{name:"Kuwait University",country:{name:"Kuwait"}}},{id:"195136",title:"Dr.",name:"Aya",middleName:null,surname:"Adel",slug:"aya-adel",fullName:"Aya Adel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/195136/images/system/195136.jpg",biography:"Dr. Adel works as an Assistant Lecturer in the unit of Phoniatrics, Department of Otolaryngology, Ain Shams University in Cairo, Egypt. Dr. Adel is especially interested in joint attention and its impairment in autism spectrum disorder",institutionString:"Ain Shams University",institution:{name:"Ain Shams University",country:{name:"Egypt"}}},{id:"94911",title:"Dr.",name:"Boulenouar",middleName:null,surname:"Mesraoua",slug:"boulenouar-mesraoua",fullName:"Boulenouar Mesraoua",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94911/images/system/94911.png",biography:"Dr Boulenouar Mesraoua is the Associate Professor of Clinical Neurology at Weill Cornell Medical College-Qatar and a Consultant Neurologist at Hamad Medical Corporation at the Neuroscience Department; He graduated as a Medical Doctor from the University of Oran, Algeria; he then moved to Belgium, the City of Liege, for a Residency in Internal Medicine and Neurology at Liege University; after getting the Belgian Board of Neurology (with high marks), he went to the National Hospital for Nervous Diseases, Queen Square, London, United Kingdom for a fellowship in Clinical Neurophysiology, under Pr Willison ; Dr Mesraoua had also further training in Epilepsy and Continuous EEG Monitoring for two years (from 2001-2003) in the Neurophysiology department of Zurich University, Switzerland, under late Pr Hans Gregor Wieser ,an internationally known epileptologist expert. \n\nDr B. Mesraoua is the Director of the Neurology Fellowship Program at the Neurology Section and an active member of the newly created Comprehensive Epilepsy Program at Hamad General Hospital, Doha, Qatar; he is also Assistant Director of the Residency Program at the Qatar Medical School. \nDr B. Mesraoua's main interests are Epilepsy, Multiple Sclerosis, and Clinical Neurology; He is the Chairman and the Organizer of the well known Qatar Epilepsy Symposium, he is running yearly for the past 14 years and which is considered a landmark in the Gulf region; He has also started last year , together with other epileptologists from Qatar, the region and elsewhere, a yearly International Epilepsy School Course, which was attended by many neurologists from the Area.\n\nInternationally, Dr Mesraoua is an active and elected member of the Commission on Eastern Mediterranean Region (EMR ) , a regional branch of the International League Against Epilepsy (ILAE), where he represents the Middle East and North Africa(MENA ) and where he holds the position of chief of the Epilepsy Epidemiology Section; Dr Mesraoua is a member of the American Academy of Neurology, the Europeen Academy of Neurology and the American Epilepsy Society.\n\nDr Mesraoua's main objectives are to encourage frequent gathering of the epileptologists/neurologists from the MENA region and the rest of the world, promote Epilepsy Teaching in the MENA Region, and encourage multicenter studies involving neurologists and epileptologists in the MENA region, particularly epilepsy epidemiological studies. \n\nDr. Mesraoua is the recipient of two research Grants, as the Lead Principal Investigator (750.000 USD and 250.000 USD) from the Qatar National Research Fund (QNRF) and the Hamad Hospital Internal Research Grant (IRGC), on the following topics : “Continuous EEG Monitoring in the ICU “ and on “Alpha-lactoalbumin , proof of concept in the treatment of epilepsy” .Dr Mesraoua is a reviewer for the journal \"seizures\" (Europeen Epilepsy Journal ) as well as dove journals ; Dr Mesraoua is the author and co-author of many peer reviewed publications and four book chapters in the field of Epilepsy and Clinical Neurology",institutionString:"Weill Cornell Medical College in Qatar",institution:{name:"Weill Cornell Medical College in Qatar",country:{name:"Qatar"}}},{id:"282429",title:"Prof.",name:"Covanis",middleName:null,surname:"Athanasios",slug:"covanis-athanasios",fullName:"Covanis Athanasios",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/282429/images/system/282429.jpg",biography:null,institutionString:"Neurology-Neurophysiology Department of the Children Hospital Agia Sophia",institution:null},{id:"190980",title:"Prof.",name:"Marwa",middleName:null,surname:"Mahmoud Saleh",slug:"marwa-mahmoud-saleh",fullName:"Marwa Mahmoud Saleh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/190980/images/system/190980.jpg",biography:"Professor Marwa Mahmoud Saleh is a doctor of medicine and currently works in the unit of Phoniatrics, Department of Otolaryngology, Ain Shams University in Cairo, Egypt. She got her doctoral degree in 1991 and her doctoral thesis was accomplished in the University of Iowa, United States. Her publications covered a multitude of topics as videokymography, cochlear implants, stuttering, and dysphagia. She has lectured Egyptian phonology for many years. Her recent research interest is joint attention in autism.",institutionString:"Ain Shams University",institution:{name:"Ain Shams University",country:{name:"Egypt"}}},{id:"259190",title:"Dr.",name:"Syed Ali Raza",middleName:null,surname:"Naqvi",slug:"syed-ali-raza-naqvi",fullName:"Syed Ali Raza Naqvi",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259190/images/system/259190.png",biography:"Dr. Naqvi is a radioanalytical chemist and is working as an associate professor of analytical chemistry in the Department of Chemistry, Government College University, Faisalabad, Pakistan. Advance separation techniques, nuclear analytical techniques and radiopharmaceutical analysis are the main courses that he is teaching to graduate and post-graduate students. In the research area, he is focusing on the development of organic- and biomolecule-based radiopharmaceuticals for diagnosis and therapy of infectious and cancerous diseases. Under the supervision of Dr. Naqvi, three students have completed their Ph.D. degrees and 41 students have completed their MS degrees. He has completed three research projects and is currently working on 2 projects entitled “Radiolabeling of fluoroquinolone derivatives for the diagnosis of deep-seated bacterial infections” and “Radiolabeled minigastrin peptides for diagnosis and therapy of NETs”. He has published about 100 research articles in international reputed journals and 7 book chapters. Pakistan Institute of Nuclear Science & Technology (PINSTECH) Islamabad, Punjab Institute of Nuclear Medicine (PINM), Faisalabad and Institute of Nuclear Medicine and Radiology (INOR) Abbottabad are the main collaborating institutes.",institutionString:"Government College University",institution:{name:"Government College University, Faisalabad",country:{name:"Pakistan"}}},{id:"58390",title:"Dr.",name:"Gyula",middleName:null,surname:"Mozsik",slug:"gyula-mozsik",fullName:"Gyula Mozsik",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/58390/images/system/58390.png",biography:"Gyula Mózsik MD, Ph.D., ScD (med), is an emeritus professor of Medicine at the First Department of Medicine, Univesity of Pécs, Hungary. He was head of this department from 1993 to 2003. His specializations are medicine, gastroenterology, clinical pharmacology, clinical nutrition, and dietetics. His research fields are biochemical pharmacological examinations in the human gastrointestinal (GI) mucosa, mechanisms of retinoids, drugs, capsaicin-sensitive afferent nerves, and innovative pharmacological, pharmaceutical, and nutritional (dietary) research in humans. He has published about 360 peer-reviewed papers, 197 book chapters, 692 abstracts, 19 monographs, and has edited 37 books. He has given about 1120 regular and review lectures. He has organized thirty-eight national and international congresses and symposia. He is the founder of the International Conference on Ulcer Research (ICUR); International Union of Pharmacology, Gastrointestinal Section (IUPHAR-GI); Brain-Gut Society symposiums, and gastrointestinal cytoprotective symposiums. He received the Andre Robert Award from IUPHAR-GI in 2014. Fifteen of his students have been appointed as full professors in Egypt, Cuba, and Hungary.",institutionString:"University of Pécs",institution:{name:"University of Pecs",country:{name:"Hungary"}}},{id:"277367",title:"M.Sc.",name:"Daniel",middleName:"Martin",surname:"Márquez López",slug:"daniel-marquez-lopez",fullName:"Daniel Márquez López",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/277367/images/7909_n.jpg",biography:"Msc Daniel Martin Márquez López has a bachelor degree in Industrial Chemical Engineering, a Master of science degree in the same área and he is a PhD candidate for the Instituto Politécnico Nacional. His Works are realted to the Green chemistry field, biolubricants, biodiesel, transesterification reactions for biodiesel production and the manipulation of oils for therapeutic purposes.",institutionString:null,institution:{name:"Instituto Politécnico Nacional",country:{name:"Mexico"}}},{id:"196544",title:"Prof.",name:"Angel",middleName:null,surname:"Catala",slug:"angel-catala",fullName:"Angel Catala",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/196544/images/system/196544.jpg",biography:"Angel Catalá studied chemistry at Universidad Nacional de La Plata, Argentina, where he received a Ph.D. in Chemistry (Biological Branch) in 1965. From 1964 to 1974, he worked as an Assistant in Biochemistry at the School of Medicine at the same university. From 1974 to 1976, he was a fellow of the National Institutes of Health (NIH) at the University of Connecticut, Health Center, USA. From 1985 to 2004, he served as a Full Professor of Biochemistry at the Universidad Nacional de La Plata. He is a member of the National Research Council (CONICET), Argentina, and the Argentine Society for Biochemistry and Molecular Biology (SAIB). His laboratory has been interested for many years in the lipid peroxidation of biological membranes from various tissues and different species. Dr. Catalá has directed twelve doctoral theses, published more than 100 papers in peer-reviewed journals, several chapters in books, and edited twelve books. He received awards at the 40th International Conference Biochemistry of Lipids 1999 in Dijon, France. He is the winner of the Bimbo Pan-American Nutrition, Food Science and Technology Award 2006 and 2012, South America, Human Nutrition, Professional Category. In 2006, he won the Bernardo Houssay award in pharmacology, in recognition of his meritorious works of research. Dr. Catalá belongs to the editorial board of several journals including Journal of Lipids; International Review of Biophysical Chemistry; Frontiers in Membrane Physiology and Biophysics; World Journal of Experimental Medicine and Biochemistry Research International; World Journal of Biological Chemistry, Diabetes, and the Pancreas; International Journal of Chronic Diseases & Therapy; and International Journal of Nutrition. He is the co-editor of The Open Biology Journal and associate editor for Oxidative Medicine and Cellular Longevity.",institutionString:"Universidad Nacional de La Plata",institution:{name:"National University of La Plata",country:{name:"Argentina"}}},{id:"186585",title:"Dr.",name:"Francisco Javier",middleName:null,surname:"Martin-Romero",slug:"francisco-javier-martin-romero",fullName:"Francisco Javier Martin-Romero",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSB3HQAW/Profile_Picture_1631258137641",biography:"Francisco Javier Martín-Romero (Javier) is a Professor of Biochemistry and Molecular Biology at the University of Extremadura, Spain. He is also a group leader at the Biomarkers Institute of Molecular Pathology. Javier received his Ph.D. in 1998 in Biochemistry and Biophysics. At the National Cancer Institute (National Institute of Health, Bethesda, MD) he worked as a research associate on the molecular biology of selenium and its role in health and disease. After postdoctoral collaborations with Carlos Gutierrez-Merino (University of Extremadura, Spain) and Dario Alessi (University of Dundee, UK), he established his own laboratory in 2008. The interest of Javier's lab is the study of cell signaling with a special focus on Ca2+ signaling, and how Ca2+ transport modulates the cytoskeleton, migration, differentiation, cell death, etc. He is especially interested in the study of Ca2+ channels, and the role of STIM1 in the initiation of pathological events.",institutionString:null,institution:{name:"University of Extremadura",country:{name:"Spain"}}},{id:"198499",title:"Dr.",name:"Daniel",middleName:null,surname:"Glossman-Mitnik",slug:"daniel-glossman-mitnik",fullName:"Daniel Glossman-Mitnik",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/198499/images/system/198499.jpeg",biography:"Dr. Daniel Glossman-Mitnik is currently a Titular Researcher at the Centro de Investigación en Materiales Avanzados (CIMAV), Chihuahua, Mexico, as well as a National Researcher of Level III at the Consejo Nacional de Ciencia y Tecnología, México. His research interest focuses on computational chemistry and molecular modeling of diverse systems of pharmacological, food, and alternative energy interests by resorting to DFT and Conceptual DFT. He has authored a coauthored more than 270 peer-reviewed papers, 32 book chapters, and 4 edited books. He has delivered speeches at many international and domestic conferences. He serves as a reviewer for more than eighty international journals, books, and research proposals as well as an editor for special issues of renowned scientific journals.",institutionString:null,institution:null},{id:"217323",title:"Prof.",name:"Guang-Jer",middleName:null,surname:"Wu",slug:"guang-jer-wu",fullName:"Guang-Jer Wu",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/217323/images/8027_n.jpg",biography:null,institutionString:null,institution:null},{id:"148546",title:"Dr.",name:"Norma Francenia",middleName:null,surname:"Santos-Sánchez",slug:"norma-francenia-santos-sanchez",fullName:"Norma Francenia Santos-Sánchez",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/148546/images/4640_n.jpg",biography:null,institutionString:null,institution:null},{id:"272889",title:"Dr.",name:"Narendra",middleName:null,surname:"Maddu",slug:"narendra-maddu",fullName:"Narendra Maddu",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/272889/images/10758_n.jpg",biography:null,institutionString:null,institution:null},{id:"242491",title:"Prof.",name:"Angelica",middleName:null,surname:"Rueda",slug:"angelica-rueda",fullName:"Angelica Rueda",position:"Investigador Cinvestav 3B",profilePictureURL:"https://mts.intechopen.com/storage/users/242491/images/6765_n.jpg",biography:null,institutionString:null,institution:null},{id:"88631",title:"Dr.",name:"Ivan",middleName:null,surname:"Petyaev",slug:"ivan-petyaev",fullName:"Ivan Petyaev",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Lycotec (United Kingdom)",country:{name:"United Kingdom"}}},{id:"428313",title:"Dr.",name:"Sambangi",middleName:null,surname:"Pratyusha",slug:"sambangi-pratyusha",fullName:"Sambangi Pratyusha",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"CGIAR",country:{name:"France"}}},{id:"423869",title:"Ms.",name:"Smita",middleName:null,surname:"Rai",slug:"smita-rai",fullName:"Smita Rai",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Integral University",country:{name:"India"}}},{id:"424024",title:"Prof.",name:"Swati",middleName:null,surname:"Sharma",slug:"swati-sharma",fullName:"Swati Sharma",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Integral University",country:{name:"India"}}},{id:"439112",title:"MSc.",name:"Touseef",middleName:null,surname:"Fatima",slug:"touseef-fatima",fullName:"Touseef Fatima",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Integral University",country:{name:"India"}}}]}},subseries:{item:{id:"94",type:"subseries",title:"Climate Change and Environmental Sustainability",keywords:"Environmental protection, Socio-economic development, Resource exploitation, Environmental degradation, Climate change, Degraded ecosystems, Biodiversity loss",scope:"\r\n\tSustainable development focuses on linking economic development with environmental protection and social development to ensure future prosperity for people and the planet. To tackle global challenges of development and environment, the United Nations General Assembly in 2015 adopted the 17 Sustainable Development Goals. SDGs emphasize that environmental sustainability should be strongly linked to socio-economic development, which should be decoupled from escalating resource use and environmental degradation for the purpose of reducing environmental stress, enhancing human welfare, and improving regional equity. Moreover, sustainable development seeks a balance between human development and decrease in ecological/environmental marginal benefits. Under the increasing stress of climate change, many environmental problems have emerged causing severe impacts at both global and local scales, driving ecosystem service reduction and biodiversity loss. Humanity’s relationship with resource exploitation and environment protection is a major global concern, as new threats to human and environmental security emerge in the Anthropocene. Currently, the world is facing significant challenges in environmental sustainability to protect global environments and to restore degraded ecosystems, while maintaining human development with regional equality. Thus, environmental sustainability with healthy natural ecosystems is critical to maintaining human prosperity in our warming planet.
",coverUrl:"https://cdn.intechopen.com/series_topics/covers/94.jpg",hasOnlineFirst:!0,hasPublishedBooks:!1,annualVolume:11978,editor:{id:"61855",title:"Dr.",name:"Yixin",middleName:null,surname:"Zhang",slug:"yixin-zhang",fullName:"Yixin Zhang",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYWJgQAO/Profile_Picture_2022-06-09T11:36:35.jpg",biography:"Professor Yixin Zhang is an aquatic ecologist with over 30 years of research and teaching experience in three continents (Asia, Europe, and North America) in Stream Ecology, Riparian Ecology, Urban Ecology, and Ecosystem Restoration and Aquatic Conservation, Human-Nature Interactions and Sustainability, Urbanization Impact on Aquatic Ecosystems. He got his Ph.D. in Animal Ecology at Umeå University in Sweden in 1998. He conducted postdoc research in stream ecology at the University of California at Santa Barbara in the USA. After that, he was a postdoc research fellow at the University of British Columbia in Canada to do research on large-scale stream experimental manipulation and watershed ecological survey in temperate rainforests of BC. He was a faculty member at the University of Hong Kong to run ecological research projects on aquatic insects, fishes, and newts in Tropical Asian streams. He also conducted research in streams, rivers, and caves in Texas, USA, to study the ecology of macroinvertebrates, big-claw river shrimp, fish, turtles, and bats. Current research interests include trophic flows across ecosystems; watershed impacts of land-use change on biodiversity and ecosystem functioning; ecological civilization and water resource management; urban ecology and urban/rural sustainable development.",institutionString:null,institution:{name:"Soochow University",institutionURL:null,country:{name:"China"}}},editorTwo:null,editorThree:null,series:{id:"24",title:"Sustainable Development",doi:"10.5772/intechopen.100361",issn:null},editorialBoard:null},onlineFirstChapters:{paginationCount:1,paginationItems:[{id:"82124",title:"Assessment of Diversity, Growth Characteristics and Aboveground Biomass of Tree Species in Selected Urban Green Areas of Osogbo, Osun State",doi:"10.5772/intechopen.104982",signatures:"Omolara Aremu, Olusola O. 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