Comparative features of privatized and public medicare (CAF Table 1.2, p. 14).
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:{caption:"Highly Cited",originalUrl:"/media/original/117"}},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"1299",leadTitle:null,fullTitle:"An Update on Glomerulopathies - Clinical and Treatment Aspects",title:"An Update on Glomerulopathies",subtitle:"Clinical and Treatment Aspects",reviewType:"peer-reviewed",abstract:"An Update on Glomerulopathies - Clinical and Treatment Aspects is a systemic overview of recent advances in clinical aspects and therapeutic options in major syndromes of glomerular pathology. The book contains twenty four chapters divided conveniently into five sections. The first section deals with primary glomerulopathies, and the second section is devoted to glomerulopathies complicating infectious conditions. The third section deals with systemic autoimmune disorders and vasculitides which constitute major causes of glomerular disease and often renal failure. The fourth section includes chapters discussing the glomerular involvement in some major metabolic and systemic conditions. The final section has chapters which relate to some general aspects of glomerular diseases. 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Prabhakar is a distinguished nephrologist currently at Texas Tech University Health Sciences Center, where he is a tenured professor in the Departments of Medicine and Cell Physiology and Molecular Biophysics, and the Chief of Nephrology Division and Vice Chairman, Department of Medicine. He is an established researcher examining pathophysiologic mechanisms of diabetic nephropathy and of insulin resistance in vitro and animal models. In the area of clinical research he initiated and is the principal investigator of a number of clinical studies. Dr. Prabhakar has over 100 publications including original articles, reviews, book chapters and published abstracts in prestigious journals, such as the American Journal of Physiology, Journal of American Society of Nephrology, and Kidney International. He has recently published a reference book entitled “Advances in the Pathogenesis of Diabetic Nephropathy”. 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Fertility and pregnancy rates decrease due to ageing in women. For this reason, it is recommended that women aged 35 and above start receiving infertility treatment after 6 months of conception attempt. After the age of 40, this period should not be waited for treatment. Many factors cause female infertility. These can be listed as medical history (family history, previous treatments, menstrual history, sexual history, etc.), physical factors (weight, body mass index, etc.), diminished ovarian reserves, ovulatory dysfunction (hypothalamic–pituitary axis (HPG axis) disorders, ovarian disorders, thyroid disorders and hyperprolactinemia, etc.), tubal factors, uterine factors and unexplained causes [2, 3]. More than 186 million people worldwide suffer from infertility, and the majority of them are residents of developing countries [4].
Kisspeptin was discovered in 1996 as the product of the kisspeptin gene (Kiss1), which is a metastatic tumour suppressor gene; therefore, it was initially called metastin [5]. Kisspeptins are a family of neuropeptides in RF-Amide structure [(neuropeptides containing arginine-phenylalanine (Arg-Phe) at the C-terminal are defined as RF-Amides)] [6]. Two years later, the connection between kisspeptin-54 and G-protein-coupled receptor-54 (GPR54) was shown for the first time [7]. In 2003, inactivating mutations of GPR54 were found in people with hypogonadotropic hypogonadism [8]. The respective receptor was previously called the GPR54, it is also identified as the kisspeptin receptor (Kiss1r) nowadays [9].
The detection of the role of the kisspeptin receptor mutation in leading to idiopathic hypogonadotropic hypogonadism paved the way for further investigations about the roles played by the kisspeptin, Kiss1, and Kiss1r systems in the field of reproductive endocrinology [10]. Many studies have shown that kisspeptin plays key roles in the regulation of different aspects of reproduction [11, 12, 13, 14, 15, 16, 17]. This review examines the possible role of kisspeptin in female infertility. In doing so, it aims to find out how future application of kisspeptin may potentially unravel the neural fertility disorder.
The Kiss1 gene encodes the neuropeptide kisspeptins. They, originally identified as metastasis suppressors, were later found to play a central regulatory role in reproduction [18]. The gene is located on human chromosome 1q32. This gene contains 2 non-expressed and 2 partially expressed regions and four exons, assembling the leader peptide consisting of 145 amino acids [19]. This precursor protein transforms into various active forms of kisspeptin with lengths of 54, 14, 13, and 10 amino acids through various post-translational modifications (Figure 1) [20]. These forms belong to the RF-amide peptide hormone family, which is closely associated with energy metabolism and reproduction. The members of the RF-amide peptide hormone family contain the common Arg-Phe-NH2 moiety at the C-terminal [21].
Amino acids sequence of human kisspeptin isoforms [
Kisspeptin receptors were first discovered in 2001 in studies about cancer, and they were named as the GPR54. Today, they are identified as the Kiss1r [9]. Kiss1r is a 396-amino acid receptor and a member of G protein-coupled receptors. The minimum length required to activate GPR54 is a 10-amino acid carboxyl terminal sequence (Kisspeptin-10) [22].
As a result of the kisspeptin binding to the GPR54/Kiss1r receptor, activates the G-protein (Gq/11) and phospholipase-C (PLC). Subsequently, diacylglycerol and inositol trisphosphate (IP3) are formed from phosphatidylinositol bisphosphate (PİP2), resulting in elevated Ca+2 concentrations. Activation of this mechanism results in the closure of the potassium channels and opening of the cation channels (TRP channels), leading to the depolarization of GnRH neurons. Consequently, GnRH neurons start secreting hormones [25]. Kisspeptin increase apoptosis and decrease cell proliferation and metastasis by stimulating the mitogen-activated protein kinase pathway (MAPK) via protein kinase C (PKC) and the extracellular signal-regulated kinase (ERK) pathway (Figure 2) [26].
Cellular action mechanism of kisspeptins [
Kisspeptin gene neurons are involved in several actions including steroid hormone feedback, metabolic signalling, and photoperiodic information regulation. It is suggested that, compatibly with their mediator role in steroid hormone feedback mechanisms, Kiss1 neurons are involved in the expression of estrogen receptors (ERα and ERβ) and progesterone receptors [21].
Kiss1 neurons are located in the periventricular nucleus (PeN), arcuate nucleus (ARC) and anteroventral periventricular nucleus (AVPV) which are located in the preoptic area of the hypothalamus (POA) in the brain and which are the regions that regulate the secretion of the GnRH hormone in mouse [28]. Kisspeptins are secreted by these nuclei. However, AVPV displays sexual dimorphism. Kiss1 mRNA expression is higher in AVPV in females compared to males. This indicates that the role of kisspeptin neurons in AVPV varies by gender [29].
The different patterns of Kiss1 mRNA regulation in the forebrain nuclei are important in the emergence of the different physiological effects of Kiss1 on the HPG axis. ARC acts as the negative feedback regulation centre for the GnRH and gonadotropin secretion, while AVPV acts as the positive feedback regulation centre responsible for the LH surge in females. ERα, ERβ, and progesterone receptors are abundant in AVPV. When these receptors bind to their ligands; they increase LH secretion, resulting in the LH surge. Furthermore, Kiss1 neurons in AVPV synapse with GnRH neurons; Kiss1 mRNA expression in AVPV peaks simultaneously with the GnRH/LH release, and the estrogen-dependent Kiss1 mRNA induction in females is involved in the GnRH/LH surge during preovulation [30]. While gonadal steroids inhibit Kiss1 neurons in ARC (negative feedback), they stimulate Kiss1 neurons in AVPV (positive feedback) [23]. Signals arising from kisspeptin binding to GPR54 receptors of the hypothalamic GnRH neurons induce the release of GnRH to the pituitary circulation. GnRH induces the release of gonadotropins (FSH, LH) from the pituitary by binding to the GnRH receptors in the pituitary gland (Figure 3) [31, 32].
Kiss1 signalling in mouse brain [
The molecular mechanisms underlying the different effects of estrogen on the Kiss1 expression in ARC and AVPV is yet to be known. However, progesterone receptors are also thought to be involved in this phenomenon. Kiss1 neurons are colocalized with or stand very close to progesterone neurons in mouse. Tyrosine hydroxylase and Kiss1 mRNAs are colocalized in AVPV but not in ARC. Consequently, it is thought that dopamine is also involved in the induction of estrogen-dependent Kiss1 expression in AVPV [33].
In mouse, ARC Kiss1 neurons synthesize Tachykinin (TAC), neurokinin-B (NKB), and dynorphin (Dyn) in variable quantities depending on species; therefore, they are also known as KNDy (Kisspeptin/Neurokinin/Dynorphin) neurons. NKB and Dyn have been shown to mutually act on kisspeptin neurosecretion [34].
The detection of the role of the kisspeptin receptor mutation in leading to idiopathic hypogonadotropic hypogonadism paved the way for studies to further investigate the other roles played by the Kisspeptin, Kiss1, and Kiss1r systems in the field of reproductive endocrinology [10]. The direct/indirect effects of kisspeptin on GnRH neurons leave no doubt that kisspeptin plays a critical role in pubertal activation. Indeed, studies on various species have shown that the Kiss1 and/or Kiss1r expression increases significantly with the onset of puberty [21]. In a study on mice, it was shown that the Kiss1 mRNA expression significantly increased in AVPV during puberty [35]. Also, centrally or peripherally administered kisspeptin in juvenile female rats shortened the timing of vaginal opening by stimulating LH release and ovulation [36, 37]. Similarly, the increase in kisspeptin-54 signal frequency in primates occur at the beginning of puberty, supporting the findings associated with the pubertal increase in kisspeptin secretion [38]. Kiss1 mRNA expression increases in ARC during puberty along with an associated increase in LH secretion in Rhesus monkeys [39].
Kisspeptin receptor damage impair normal sexual development and to result in the failure of starting puberty. Despite the synthesis of GnRH at normal levels in the hypothalamic GnRH neurons, LH/FSH secretions do not occur and pituitary gonadotropic cells remain unresponsive to externally administered GnRH in such cases [40]. The emergence of problems in the process of starting puberty in the presence of kisspeptin deficiencies has led to the idea that kisspeptin may be an important factor for the start of sexual maturation. This idea has been confirmed by significantly increased levels of released GnRH via kisspeptin injections in mammals and by the acceleration of pubertal start via repeated Kisspeptin injections in juvenile rats. Thus, it has been proven that Kisspeptin certainly participates in pubertal development [41].
A cerebral antibody binds and inactivates kisspeptin in the female rats, impairing or even stopping reproductive functions. Also, the administration of kisspeptin in fasted rats sustains the release of GnRH and that mammals suspend their reproductive functions during states of long-term hunger in order to spend energy only enough to maintain physiological requirements. Nonetheless, the administration of kisspeptin reverses this natural process and restarts reproductive functions [42].
Nitric oxide (NO) is another potential mediator that can affect the onset of puberty since it is a mediator involved in several vital functions such as gonadotropin release, steroidogenesis, folliculogenesis, ovulation, luteal development, luteolysis, and pregnancy [43, 44]. Neuronal nitric oxide synthase (nNOS) is one of the three forms of an enzyme that oxidizes L-arginine to L-citrulline and NO. nNOS neurons in mice and rats contain high densities of ERα [45]. In rats, NO stimulates LH and GnRH release. In mice, deletion of nNOS causes infertility and hypogonadism [46]. Furthermore, recent evidence suggests that kisspeptin may directly act on the release of NO. In adult female mice, kisspeptin close-contacts to nNOS neurons have been observed in the ARC and preoptic region; however, Kiss1r is expressed only from nNOS neurons in the preoptic region [47].
Kisspeptin and neurokinin-B agonists can be used to stimulate the HPG axis in conditions associated with infertility due to central nervous system causes if the system of GnRH neurons is intact. Kisspeptin and neurokinin-B may offer a novel therapeutic approach to treat failures associated with increased/reduced gonadotropin pulsatile secretion. Kisspeptins may be associated with a lower risk of ovarian hyperstimulation syndrome (OHSS) compared to human chorionic gonadotropin (hCG) injections [48]. In polycystic ovary syndrome (PCOS), kisspeptin antagonists can help normalize LH hypersecretion along with ovulation and follicular development [49].
In a study on patients with unexplained infertility (UI), PCOS, and male factor infertility (MFI); In PCOS group kisspeptin levels were measured and found to be significantly higher compared to the MFI and UI groups. The investigators suggested that IU can be treated with kisspeptin injections and that high kisspeptin levels can be a reliable indicator to estimate the antral follicle count (AFC) and to diagnose PCOS [50].
In women with functional hypothalamic amenorrhea (HA) due to low body weight, the administration of kisspeptin-54 acutely stimulates secretion of gonadotropin and that the effect on gonadotropin secretion is significant after the first injection but diminishes considerably (tachyphylaxis) after injections for two weeks [51]. Nevertheless, the frequency of injections was changed from twice a day to twice a week in another study, and gonadotropin response was sustained [52]. Eight-hour intravenous infusion of kisspeptin-54 has been shown to temporarily increase LH pulse frequency and amplitude in women with hypothalamic amenorrhea [53].
Hyperprolactinemia is one of the leading causes of female infertility as it causes hypogonadotropic anovulation [54]. Since kisspeptin neurons have recently been shown to express prolactin receptors, kisspeptin has been identified as the key mediator involved in this system [55]. In mice, hyperprolactinemia causes anovulation through decreased gonadotropin and GnRH secretion and low levels of kisspeptin expression. Kisspeptin administration in these mice repairs ovarian cycle and gonadotropin secretion. It suggests that kisspeptin neurons have a role in hyperprolactinemic anovulation [56].
Endometriosis is a disease that causes infertility in women [57]. A study conducted in 2012 about endometriosis reported that Kiss1 expression could not be detected in any sample taken from endometriosis patients [58]. In one study, researchers found that the level of Kiss1 expression was statistically significantly higher in endometriosis lesions compared to the level determined in eutopic glandular endometrium and concluded that Kiss1 might have a possible role in the pathogenesis of endometriosis [59]. Another study reported that Kiss1r mRNA levels were statistically significantly higher in the cumulus cells of endometriosis patients compared to healthy oocyte donors. In consequence, researchers argue that the increased Kiss1r expression may be one of the many factors involved in the root cause of endometriosis and related infertility [60].
A study in women suffering from infertility, investigating the genetic association between the neurokinin (TAC3/TAC3R) systems and kisspeptin (Kiss1/Kiss1r) and investigating the expression of these systems, found that the expression of Kiss1, TAC3, and TAC3R was downregulated in the cumulus cells. Similarly, these three genes have been reported to be downregulated in older women with age-related infertility [60]. In that study, these findings could only be attributed to age because infertile patients were significantly older than healthy donors and because the endometriosis patients were younger and showed just an opposite expression profile compared to all other patients, including patients with age-related infertility and low responders [61].
This review has examined the association of kisspeptin with female infertility and concluded that kisspeptin has a key role in the HPG axis and can be potentially used for the treatment of reproductive disorders including hypogonadism, ovarian hyperstimulation syndrome (OHSS), polycystic ovary syndrome (PCOS), unexplained infertility (UI), male factor infertility (MFI), hypothalamic amenorrhea (HA), and endometriosis. The literature review revealed that no adverse effects were reported after kisspeptin administration in healthy individuals and patients. Therefore, kisspeptin can be used safely in both healthy and infertile individuals. Especially its positive effects on GnRH and its key role in the initiation of physiological events in the hypothalamic–pituitary-gonadal axis (HPG axis) show that kisspeptin has a say in fertility. For this reason, kisspeptin is an option that should be focused on in the solution of infertility cases that develop in mammals (humans and especially livestock) and are one of the diseases of the age.
This is the U.S. story—from the birth of health insurance responding to genuine human need in the depths of the Great Depression in the 1930s—to the opulence of a massive corporatized industry today exploiting that need all the way to the bank. How do we explain that turn-around? This chapter has four goals: (1) to bring some historical perspective to that question; (2) to briefly summarize how health care services are bought and paid for in the U.S.; (3) to describe how private health insurance and multi-payer financing have failed the public interest; and (4) to compare four reform alternatives currently under consideration, only one of which will bring lasting reform through universal coverage.
Some in the U.S. considered the possibility of compulsory health insurance early in the 20th century after noting that 10 European countries had adopted one or another form of it by 1913 [1]. But that idea was controversial, and the emergence of voluntary, private health insurance in this country is especially attributed to a Blue Cross plan for school teachers in Dallas, Texas, in 1929. At that time as the Great Depression took hold, the nation’s hospitals were in dire straits with more than one-third of the general hospital beds empty [2].
As the prototype upon which later Blue Cross plans were based, the Baylor plan provided free hospitalization for up to 21 days as well as coverage for operating room, laboratory and anesthesia services. The hospital assumed financial risk for hospital care without any third party and collected pre-payments. Other prepaid health insurance plans were soon to follow. The World War II years saw the start of employer-sponsored health insurance, when employers found it helpful to offer health insurance in order to recruit workers during a wartime economy with a severe labor shortage. By 1950, more than one-half of Americans were covered for the first time [3].
In the last 60-plus years, the private health insurance industry has been transformed from the quasi private-public partnership of its pioneering years to a massive industry on a corporate mission of profit over service. It has followed a conventional theory of insurance based on the concept of “moral hazard,” whereby those with insurance are expected to overuse health care services and lead to uncontrolled increases in health care costs. As a result, community rating and guaranteed coverage during earlier years gave way to experience rating as medical underwriting became the new norm. The Blues were under pressure to compromise their earlier service mission, so that one-half of the nation’s Blue Cross Blue Shield plans had consolidated and converted into for-profit companies by 2005 [4].
With some 1300 private insurers, the risk pool has fragmented into ever smaller parts as insurers work to avoid adverse selection. Medicare and Medicaid were enacted in 1965 as public plans, but recent decades have seen their increasing privatization that often ends up leaving many enrollees uninsured.
These are some of the many ways that insurers have used to extract more income at the expense of reliable and affordable coverage for enrollees:
“Denial management” became a growth industry of its own aimed at denying physicians’ and hospitals’ claims for services provided [5]. Many insurers developed ways of avoiding coverage of higher risk people in the first place. One such technique was to hold marketing meetings on the second floor of buildings without elevators to discourage less mobile and older people. Another technique was to make steep increases in premiums after receiving claims from enrollees who were sicker than expected. Denial of claims through burdensome pre-authorization of service became still another way to avoid paying expensive claims, increasingly associated with ever-changing networks. Out-of-network claims for hospital and physicians’ services became unaffordable for many enrollees; even for in-network claims, the average denial rate today is 18% [6].
Managed care grew rapidly during and after the 1990s, as a way to contain health care costs by changing from fee-for-service payment to prospective payment based upon capitation—the number of individuals enrolled in a health maintenance organization (HMO) plan. That gave insurers yet another way to profit from providing less care, and soon became known as managed
Insurers have increasingly privatized Medicare and Medicaid in recent years as ways to exploit federal funding sources. Their claims that privatization would be more efficient have been proven false by experience. Instead, they have been more restrictive in choice and coverage, increased their administrative overhead to five or six times higher than traditional Medicare, and left markets that were insufficiently profitable. They have also increased their revenues by up-coding diagnoses—claiming payment for conditions for which care was not provided [8]. Table 1 shows marked differences between privatized Medicare and traditional public Medicare by the early 2000s [9].
Privatized medicare | Original medicare |
---|---|
Experience-rated eligibility | Universal coverage |
Managed competition | Social insurance as earned right |
Defined contribution | Defined benefits |
Segmented risk pool | Broad risk pool |
Market pricing to risk | Administered prices |
More volatile access & benefits | More reliable access & benefits |
Increased cost sharing | Less cost sharing |
Less accountability | Potential for more accountability |
Less choice of provider & hospital | Full choice of provider & hospital |
Less well distributed | Well distributed |
Less efficiency, higher overhead | More efficiency, lower overhead |
Comparative features of privatized and public medicare (CAF Table 1.2, p. 14).
Source: Geyman [9].
Increasing consolidation through mergers within the private health insurance industry has taken place since the 1990s. The largest insurers today—in numeric order United Health Group, Anthem, Aetna and Cigna—collectively have a market share of 49% [10]. As a result, that level of consolidation has led to less competition, more cost sharing with higher deductibles, and less options for enrollees. United Health Group, as the largest insurer in the country, has also gained clout beyond insurance by selling technology to hospitals, managing clinical trials, distributing prescription drugs, and offering continuing medical education to physicians [11].
Before looking at the role of private health insurance in U.S. health care, it is helpful (though still confusing!) to ask who really pays for health care. The late Dr. Uwe Reinhardt, Professor of Political Economy at Princeton University and author of
Who pays for health care, and how is it paid (Figure 9.6, CAF 128).
Today’s system of paying for health care works against most of the working population through what economists call “labor income”—what people earn in their everyday jobs— that is taxed higher than “capital income” (accumulated wealth). As a result, billionaires today pay lower tax rates than their secretaries, steel workers, school teachers, and retirees [13].
These are some of the ways in which private health insurance and multi-payer financing have failed the common good in this country.
Our market-driven system, now consolidated to a small number of corporate giants, can charge what the market will bear. Predictably, the cost of medical care has doubled compared to the consumer-price index over the last 25 years [14]. Figure 2 shows the cumulative growth of the cost of premiums for employer-sponsored health insurance compared to annual average earnings of the bottom 90% over the last 20 years [15]. As a result, four in ten people with that insurance do not have enough savings to cover the deductibles and one in six have to cut back on food, take an extra job, or move in with friends or family [16]. Even when insured, many enrollees defer or avoid needed care, while many others receive high surprise medical bills that drag them into poverty, often ending them up in medical bankruptcy [17].
(Figure 7.2 MIC 104).
Predictably, increased cost sharing cuts access to care ranging from ER visits and office visits to hospital care and mental health [18]. As Dr. Veena Shankaran of the Hutchinson Cancer Research Center observes:
Private insurers have many ways to game the system at the expense of patients and taxpayers. Even after passage of the Affordable Care Act (ACA) in 2010, they discriminate against the sick by such benefit designs that limit access, high cost-sharing, restrictive drug formularies, inadequate and ever-changing networks of physicians and hospitals, and deceptive marketing practices. Meanwhile, they market new kinds of inadequate gap insurance, immune from the ACA’s requirements, that include, for example, copays for treatment and lump sum payments upon diagnosis of such conditions as cancer, heart disease and stroke [20]. Short-term plans are another way to evade the ACA’s requirements, providing very limited coverage for up to 1 year at exorbitant costs. Correctly labeled as “junk insurance,” the aptly named Golden Rule Insurance has brought big profits to its owner, the giant United Health Group [21].
Private insurers consume 15–20% of the health care dollar in bureaucracy, administrative overhead, and profits. Figure 3 shows how much higher that overhead is compared to other countries [22]. At the same time, they have received large subsidies from the federal government for many years, now about $685 billion a year [23] and projected by the Congressional Budget Office to double in another 10 years [24].
Insurance overhead in 6 countries (CAF Figure 11.2, 151).
Overpayments for privatized Medicare and Medicaid have been a bonanza for private insurers, accounting for more than one-half of their net revenue. Their fraudulent practice of up-coding, mentioned above, accounts for much of that revenue, as shown in Figure 4 [25].
(CAF Figure 4.2, 45).
Wall Street investors have much to say about what private insurers do in their unending quest for more profits. As one example, CVS Health, the parent company of Aetna, made far more money in 2021 than most other publicly traded corporations, in part because of Aetna’s jacking up premiums and cost sharing, which it will do again in 2022. When the company issued a guidance for 2022 profits of just $12 billion to $13 billion (down just slightly from that for 2021 of $12.5 to $13 billion), its share price dropped by 6%, unnerving investors, and the company proceeded to buy back its own shares to boost earnings per share. Aetna’s health insurance market has going down due to the decline of employer-sponsored health insurance, with less than one-third of businesses with 50 or fewer employees now offering health benefits [26].
Stepping back to consider all of this, Gerald Friedman, PhD, Professor of Economics at the University of Massachusetts Amherst and author of
Despite receiving long-term subsidies from the federal government, private health insurers leave their market, often with little advance notice, whenever their profits fall below expectations of their CEOs and shareholders. As just one example, at least 1.4 million people in 32 states lost their ACA coverage at the end of 2016, leaving them fewer choices than before [28].
To be effective nationally, health insurance must be compulsory in order to eliminate segmentation of risk pools, as Dr. Henry Sigerist, then Director of the History of Medicine at the Johns Hopkins University, recognized as far back as 1944:
The above account of the expensive missteps in U.S. health insurance over these many years shows how important universal coverage is to meet the needs of our population, as has been shown in many advanced countries around the world. Remarkably, a proposal was made for national health insurance by Teddy Roosevelt as a presidential candidate on the progressive ticket more than a century ago in 1912. It was rejected then and thereafter as the political debate became controlled by corporate stakeholders in the present lucrative financing “system.” With health care now accounting for more than one-sixth of the nation’s GDP, corporate power and lobbying for its continuance have continued to block reform efforts for cost containment, health care equity, and universal coverage. It has become increasingly clear that employer-sponsored health insurance has itself been a big part of the problem, as Drs. Anne Case and Angus Deaton, Professors Emeritus of Economics and Public Affairs at Princeton University recently observed:
Health care has become a front-burner issue in recent political campaigns and as we head into the 2022 and 2024 election cycles. These four reform alternatives are up for debate:
Building on the Affordable Care Act (ACA) of 2010;
Medicare for Some: increasing the numbers of insured by Medicare by lowering the eligibility age to 60, together with a public option for sale alongside private plans on the ACA’s exchanges;
Privatized Medicare Advantage for All; and
Single-payer Medicare for All.
The first three of these alternatives would leave a for-profit, multi-payer financing system in place with all of the problems described previously. The fourth alternative is the only one that can bring a not-for-profit public financing system with universal coverage for all Americans, cost containment, improved access and quality of care. There is a bill in the House of Representatives (H. R. 1976) for Medicare for All with more than 120 co-sponsors. However, the Congress is sharply divided along partisan lines, and this bill may have to wait for the forthcoming elections for the Congress to clarify its priorities.
Although much of organized medicine in the U.S. has opposed national health insurance over the years, that stance is beginning to change as so many physicians find our present multi-payer financing system such an impediment to daily medical practice. Medicare for All already has strong support among the general public, physicians and nurses. Experience and evidence over the years confirms its advantages as shown by Table 2 [31]. Had Medicare for All been in place during 2019, it is estimated that we would have saved more than $1 trillion. Figure 5 shows how those savings would have been taken place [32].
ACA | Public option | Medicare advantage for all | Medicare for all | |
---|---|---|---|---|
Access | Restricted | Restricted | Restricted | Unrestricted |
Choice | Restricted | Restricted | Restricted | Unrestricted |
Cost containment | Never | Never | Never | Yes |
Quality of care | Unacceptable | Unacceptable | Unacceptable | Improved |
Bureaucracy | Large, wasteful | Large, wasteful | Large, wasteful | Much reduced |
Universal coverage | Never | Never | Never | Yes |
Accountability | No | No | No | Yes |
Sustainability | No | No | No | Yes |
Comparison of four reform alternatives based on evidence (Table 13.1, 60 years, 160).
Medicare for all savings compared to current system, 2019 (Figure 14.2, MIC 269).
If and when Medicare for All can be enacted, it will bring a new system of national health insurance for all Americans with comprehensive benefits based on medical need, not ability to pay, together with full choice of hospitals, physicians and other health professionals anywhere in the country. Administrative simplification will drop its single-payer overhead to about 3%, one-sixth of today’s multi-payer overhead. Cost savings will be achieved through large-scale cost controls, including (a) negotiated fee schedules for physicians and other health professionals, who will remain in private practice; (b) global annual budgeting of hospitals and other facilities; and (c) bulk purchasing of drugs and medical devices. Cost sharing through deductibles and copayments will be eliminated at the point of service, and pre-authorization of services will no longer be needed. Higher priority will be given to primary care and public health, while the risk for costs of illness and accidents will be shared across our entire population of 330 million Americans.
The corporate transformation of health care in this country from a traditional service ethic to a commodity for sale in an unfettered marketplace is indeed unfortunate. Financing reform through a not-for-profit public mechanism—Medicare for All—can go a long way to restoring the traditional service ethic of health care as a moral enterprise. We shall see what the future will bring. Meanwhile, Winston Churchill gives us hope:
We believe financial barriers should not prevent researchers from publishing their findings. With the need to make scientific research more publicly available and support the benefits of Open Access, more and more institutions and funders are dedicating resources to assist faculty members and researchers cover Open Access Publishing Fees (OAPFs). In addition, IntechOpen provides several further options presented below, all of which are available to researchers, and could secure the financing of your Open Access publication.
",metaTitle:"Waiver Policy",metaDescription:"We feel that financial barriers should never prevent researchers from publishing their research. With the need to make scientific research more publically available and support the benefits of Open Access, more institutions and funders have dedicated funds to assist their faculty members and researchers cover the APCs associated with publishing in Open Access. Below we have outlined several options available to secure financing for your Open Access publication.",metaKeywords:null,canonicalURL:"/page/waiver-policy",contentRaw:'[{"type":"htmlEditorComponent","content":"At IntechOpen, the majority of OAPFs are paid by an Author’s institution or funding agency - Institutions (73%) vs. Authors (23%).
\\n\\nThe first step in obtaining funds for your Open Access publication begins with your institution or library. IntechOpen’s publishing standards align with most institutional funding programs. Our advice is to petition your institution for help in financing your Open Access publication.
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\\n\\nFor Authors who are unable to obtain funding from their institution or research funding bodies and still need help in covering publication costs, IntechOpen offers the possibility of applying for a Waiver.
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\\n\\nThe application process is open after your submitted manuscript has been accepted for publication. To apply, please fill out a Waiver Request Form and send it to your Author Service Manager. If you have an official letter from your university or institution showing that funds for your OA publication are unavailable, please attach that as well. The Waiver Request will normally be addressed within one week from the application date. All chapters that receive waivers or partial waivers will be designated as such online.
\\n\\nDownload Waiver Request Form
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'At IntechOpen, the majority of OAPFs are paid by an Author’s institution or funding agency - Institutions (73%) vs. Authors (23%).
\n\nThe first step in obtaining funds for your Open Access publication begins with your institution or library. IntechOpen’s publishing standards align with most institutional funding programs. Our advice is to petition your institution for help in financing your Open Access publication.
\n\nHowever, as Open Access becomes a more commonly used publishing option for the dissemination of scientific and scholarly content, in addition to institutions, there are a growing number of funders who allow the use of grants for covering OA publication costs, or have established separate funds for the same purpose.
\n\nPlease consult our Open Access Funding page to explore some of these funding opportunities and learn more about how you could finance your IntechOpen publication. Keep in mind that this list is not definitive, and while we are constantly updating and informing our Authors of new funding opportunities, we recommend that you always check with your institution first.
\n\nFor Authors who are unable to obtain funding from their institution or research funding bodies and still need help in covering publication costs, IntechOpen offers the possibility of applying for a Waiver.
\n\nOur mission is to support Authors in publishing their research and making an impact within the scientific community. Currently, 14% of Authors receive full waivers and 6% receive partial waivers.
\n\nWhile providing support and advice to all our international Authors, waiver priority will be given to those Authors who reside in countries that are classified by the World Bank as low-income economies. In this way, we can help ensure that the scientific work being carried out can make an impact within the worldwide scientific community, no matter where an Author might live.
\n\nThe application process is open after your submitted manuscript has been accepted for publication. To apply, please fill out a Waiver Request Form and send it to your Author Service Manager. If you have an official letter from your university or institution showing that funds for your OA publication are unavailable, please attach that as well. The Waiver Request will normally be addressed within one week from the application date. All chapters that receive waivers or partial waivers will be designated as such online.
\n\nDownload Waiver Request Form
\n\nFeel free to contact us at funders@intechopen.com if you have any questions about Funding options or our Waiver program. If you have already begun the process and require further assistance, please contact your Author Service Manager, who is there to assist you!
\n\nNote: All data represented above was collected by IntechOpen from 2013 to 2017.
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Cells encode “receptors” containing Ub-/Ubl-binding domains that interpret and translate each modification into appropriate cellular responses. Among the different Ubls, NEDD8, which is the ubiquitin’s closest relative, retains many of the structural determinants that enable ubiquitin the ability to target proteins to degradation. Nevertheless, the direct involvement of NEDD8 conjugation to proteasome recruitment has been proved only in a few cases. To date, well-defined major NEDD8 substrates are primarily members of the cullin family, and cullin neddylation does not appear to mark these proteins for degradation. Various studies have demonstrated that selectivity between ubiquitin and NEDD8 is guaranteed by small but substantial differences. Nevertheless, several issues still need to be addressed, mainly concerning which interaction surfaces mediate NEDD8 function and what domains recognize them. Recently, two novel domains identified in KHNYN and N4BP1 proteins have shed new light on this research area. Here, I discuss some recent reports that contributed to shed light on the mechanisms underlining the discrimination between ubiquitin and NEDD8. Understanding the details of these molecular mechanisms represents a prominent facet for the identification of new therapeutic targets.",book:{id:"8301",slug:"ubiquitin-proteasome-system-current-insights-into-mechanism-cellular-regulation-and-disease",title:"Ubiquitin Proteasome System",fullTitle:"Ubiquitin Proteasome System - Current Insights into Mechanism Cellular Regulation and Disease"},signatures:"Elena Santonico",authors:[{id:"271923",title:"Dr.",name:"Elena",middleName:null,surname:"Santonico",slug:"elena-santonico",fullName:"Elena Santonico"}]},{id:"28199",doi:"10.5772/31082",title:"F0F1 ATP Synthase: A Fascinating Challenge for Proteomics",slug:"f0f1-atp-synthase-a-fascinating-challenge-for-proteomics",totalDownloads:5557,totalCrossrefCites:2,totalDimensionsCites:8,abstract:null,book:{id:"780",slug:"proteomics-human-diseases-and-protein-functions",title:"Proteomics",fullTitle:"Proteomics - Human Diseases and Protein Functions"},signatures:"Federica Dabbeni-Sala, Amit Kumar Rai and Giovanna Lippe",authors:[{id:"85523",title:"Prof.",name:"Giovanna",middleName:null,surname:"Lippe",slug:"giovanna-lippe",fullName:"Giovanna Lippe"},{id:"149272",title:"Dr.",name:"Federica",middleName:null,surname:"Dabbeni-Sala",slug:"federica-dabbeni-sala",fullName:"Federica Dabbeni-Sala"},{id:"149273",title:"Dr.",name:"Amit",middleName:null,surname:"Kumar Rai",slug:"amit-kumar-rai",fullName:"Amit Kumar Rai"}]},{id:"65025",doi:"10.5772/intechopen.82883",title:"E3 Ubiquitin Ligases in Cancer and Their Pharmacological Targeting",slug:"e3-ubiquitin-ligases-in-cancer-and-their-pharmacological-targeting",totalDownloads:1681,totalCrossrefCites:2,totalDimensionsCites:8,abstract:"Ubiquitination plays many critical roles in protein function and regulation. Consequently, mutation and aberrant expression of E3 ubiquitin ligases can drive cancer progression. Identifying key ligase-substrate relationships is crucial to understanding the molecular basis and pathways behind cancer and toward identifying novel targets for cancer therapeutics. Here, we review the importance of E3 ligases in the regulating the hallmarks of cancer, discuss some of the key and novel E3 ubiquitin ligases that drive tumor formation and angiogenesis, and review the clinical development of inhibitors that antagonize their function. We conclude with perspectives on the field and future directions toward understanding ubiquitination and cancer progression.",book:{id:"8301",slug:"ubiquitin-proteasome-system-current-insights-into-mechanism-cellular-regulation-and-disease",title:"Ubiquitin Proteasome System",fullTitle:"Ubiquitin Proteasome System - Current Insights into Mechanism Cellular Regulation and Disease"},signatures:"Joseph Y. Ong and Jorge Z. Torres",authors:[{id:"186645",title:"Dr.",name:"Jorge",middleName:null,surname:"Torres",slug:"jorge-torres",fullName:"Jorge Torres"},{id:"264944",title:"Mr.",name:"Joseph",middleName:null,surname:"Ong",slug:"joseph-ong",fullName:"Joseph Ong"}]},{id:"28201",doi:"10.5772/31113",title:"Identification of the Novel Plasminogen Receptor, Plg-RKT",slug:"identification-of-the-novel-plasminogen-receptor-plg-rkt",totalDownloads:2435,totalCrossrefCites:2,totalDimensionsCites:5,abstract:null,book:{id:"780",slug:"proteomics-human-diseases-and-protein-functions",title:"Proteomics",fullTitle:"Proteomics - Human Diseases and Protein Functions"},signatures:"Lindsey A. Miles, Nicholas M. Andronicos, Emily I. Chen, Nagyung Baik, Hongdong Bai, Caitlin M. Parmer, Shahrzad Lighvani, Samir Nangia, William B. Kiosses, Mark P. Kamps, John R. Yates III and Robert J. Parmer",authors:[{id:"85634",title:"Dr.",name:"Lindsey A.",middleName:null,surname:"Miles",slug:"lindsey-a.-miles",fullName:"Lindsey A. Miles"},{id:"85772",title:"Dr.",name:"Nicholas M.",middleName:null,surname:"Andronicos",slug:"nicholas-m.-andronicos",fullName:"Nicholas M. Andronicos"},{id:"85773",title:"Dr.",name:"Emily I.",middleName:null,surname:"Chen",slug:"emily-i.-chen",fullName:"Emily I. Chen"},{id:"85775",title:"MSc.",name:"Nagyung",middleName:null,surname:"Baik",slug:"nagyung-baik",fullName:"Nagyung Baik"},{id:"85776",title:"Dr.",name:"Hongdong",middleName:null,surname:"Bai",slug:"hongdong-bai",fullName:"Hongdong Bai"},{id:"85777",title:"Ms.",name:"Caitlin M.",middleName:null,surname:"Parmer",slug:"caitlin-m.-parmer",fullName:"Caitlin M. Parmer"},{id:"85778",title:"Dr.",name:"William B.",middleName:null,surname:"Kiosses",slug:"william-b.-kiosses",fullName:"William B. Kiosses"},{id:"85780",title:"Dr.",name:"John R.",middleName:null,surname:"Yates, III",slug:"john-r.-yates-iii",fullName:"John R. Yates, III"},{id:"85781",title:"Dr.",name:"Robert J.",middleName:null,surname:"Parmer",slug:"robert-j.-parmer",fullName:"Robert J. Parmer"},{id:"123594",title:"Dr.",name:"Samir",middleName:null,surname:"Nangia",slug:"samir-nangia",fullName:"Samir Nangia"},{id:"123595",title:"Dr.",name:"Shahrzad",middleName:null,surname:"Lighvani",slug:"shahrzad-lighvani",fullName:"Shahrzad Lighvani"}]}],mostDownloadedChaptersLast30Days:[{id:"70577",title:"Proteoforms: General Concepts and Methodological Process for Identification",slug:"proteoforms-general-concepts-and-methodological-process-for-identification",totalDownloads:924,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"The term proteoform is used to denote all the molecular forms in which the protein product of a single gene can be found. The most frequent processes that lead to transcript modification and the biological implications of these changes observed in the final protein product will be discussed. Proteoforms arising from genetic variations, alternatively spliced RNA transcripts and post-translational modifications will be commented. This chapter will present an evolution of the techniques used to identify the proteoforms and the importance of this identification for understanding of biological processes. This chapter highlights the fundamental concepts in the field of top-down mass spectrometry (TDMS), and provides numerous examples for the use of knowledge obtained from the identification of proteoforms. The identification of mutant proteins is one of the emerging areas of proteogenomics and has the potential to recognize novel disease biomarkers and may point to useful targets for identification of therapeutic approaches.",book:{id:"9352",slug:"proteoforms-concept-and-applications-in-medical-sciences",title:"Proteoforms",fullTitle:"Proteoforms - Concept and Applications in Medical Sciences"},signatures:"Jucélia da Silva Araújo and Olga Lima Tavares Machado",authors:[{id:"30130",title:"Dr.",name:"Olga Lima Tavares",middleName:null,surname:"Machado",slug:"olga-lima-tavares-machado",fullName:"Olga Lima Tavares Machado"},{id:"310148",title:"Dr.",name:"Jucelia",middleName:null,surname:"Da Silva Araujo",slug:"jucelia-da-silva-araujo",fullName:"Jucelia Da Silva Araujo"}]},{id:"65025",title:"E3 Ubiquitin Ligases in Cancer and Their Pharmacological Targeting",slug:"e3-ubiquitin-ligases-in-cancer-and-their-pharmacological-targeting",totalDownloads:1681,totalCrossrefCites:2,totalDimensionsCites:8,abstract:"Ubiquitination plays many critical roles in protein function and regulation. Consequently, mutation and aberrant expression of E3 ubiquitin ligases can drive cancer progression. Identifying key ligase-substrate relationships is crucial to understanding the molecular basis and pathways behind cancer and toward identifying novel targets for cancer therapeutics. Here, we review the importance of E3 ligases in the regulating the hallmarks of cancer, discuss some of the key and novel E3 ubiquitin ligases that drive tumor formation and angiogenesis, and review the clinical development of inhibitors that antagonize their function. We conclude with perspectives on the field and future directions toward understanding ubiquitination and cancer progression.",book:{id:"8301",slug:"ubiquitin-proteasome-system-current-insights-into-mechanism-cellular-regulation-and-disease",title:"Ubiquitin Proteasome System",fullTitle:"Ubiquitin Proteasome System - Current Insights into Mechanism Cellular Regulation and Disease"},signatures:"Joseph Y. Ong and Jorge Z. Torres",authors:[{id:"186645",title:"Dr.",name:"Jorge",middleName:null,surname:"Torres",slug:"jorge-torres",fullName:"Jorge Torres"},{id:"264944",title:"Mr.",name:"Joseph",middleName:null,surname:"Ong",slug:"joseph-ong",fullName:"Joseph Ong"}]},{id:"65109",title:"Ubiquitin Signaling in Regulation of the Start of the Cell Cycle",slug:"ubiquitin-signaling-in-regulation-of-the-start-of-the-cell-cycle",totalDownloads:1578,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"The small protein ubiquitin plays a vital role in virtually all aspects of cellular life. Among the diverse signaling outcomes associated with ubiquitination, the most well-established is the targeted degradation of substrates via the proteasome. During cell growth and proliferation, ubiquitin plays an outsized role in promoting progression through the cell cycle. In particular, ubiquitin-mediated degradation is critically important at transition points where it provides directionality and irreversibility to the cell cycle, which is essential for maintaining genome integrity. Specifically, the boundary between G1 and S-phase is tightly regulated by the ubiquitin proteasome system. Notably, the G1/S boundary represents a major barrier to cell proliferation and is universally dysfunctional in cancer cells, allowing for the unbridled proliferation observed in malignancy. Numerous E3 ubiquitin ligases, which facilitate the ubiquitination of specific substrates, have been shown to control G1/S. In this chapter, we will discuss components in the ubiquitin proteasome system that are implicated in G1/S control, how these enzymes are interconnected, gaps in our current knowledge, and the potential role of these pathways in the cancer cycle and disease proliferation.",book:{id:"8301",slug:"ubiquitin-proteasome-system-current-insights-into-mechanism-cellular-regulation-and-disease",title:"Ubiquitin Proteasome System",fullTitle:"Ubiquitin Proteasome System - Current Insights into Mechanism Cellular Regulation and Disease"},signatures:"Michael James Emanuele and Taylor Paige Enrico",authors:[{id:"264977",title:"Dr.",name:"Michael",middleName:null,surname:"Emanuele",slug:"michael-emanuele",fullName:"Michael Emanuele"},{id:"282200",title:"Ms.",name:"Taylor",middleName:null,surname:"Enrico",slug:"taylor-enrico",fullName:"Taylor Enrico"}]},{id:"60432",title:"Protein-Based Detection Methods for Genetically Modified Crops",slug:"protein-based-detection-methods-for-genetically-modified-crops",totalDownloads:1430,totalCrossrefCites:3,totalDimensionsCites:4,abstract:"The generation of genetically modified (GM) crops is rapidly expanding each and every year around the world. The well-being and quality assessment of these harvests are vital issues with respect to buyers’ interests. This drove the administrative specialists to execute an arrangement of extremely strict strategies for the endorsement to develop and use GMOs and to produce an interest in scientific techniques equipped for identifying GM crops. The GM crops have been added to the effective fuse of various attributes by presenting transgenes, for example, Bacillus thuringiensis (Bt) insecticidal qualities, in various crop species. GM crops give critical financial, natural, well-being and social advantages to both small and large agriculturists. The detection strategies incorporate either DNA-based or protein-based measures. Different immunoassays or catalyst connected immunosorbent tests are delicate and more affordable; however, they need experienced technicians. A very simple method, that is, immunochromatographic (ICS) test, is set up in the world, which is modest, compact and simple to utilize. The ICS is a semiquantitative method for indicative screening and semi-measurement of new remote proteins presented through hereditary change of plants. The strip is the easiest method for the assessment of several Bt crop plants for insecticidal quality.",book:{id:"6635",slug:"protein-protein-interaction-assays",title:"Protein-Protein Interaction Assays",fullTitle:"Protein-Protein Interaction Assays"},signatures:"Kausar Malik, Haleema Sadia and Muhammad Hamza Basit",authors:[{id:"238750",title:"Prof.",name:"Kausar",middleName:null,surname:"Malik",slug:"kausar-malik",fullName:"Kausar Malik"},{id:"243713",title:"Dr.",name:"Haleema",middleName:null,surname:"Sadia",slug:"haleema-sadia",fullName:"Haleema Sadia"},{id:"243714",title:"Mr.",name:"Muhammad Hamza",middleName:null,surname:"Basit",slug:"muhammad-hamza-basit",fullName:"Muhammad Hamza Basit"}]},{id:"60064",title:"Rapid Endosomal Recycling",slug:"rapid-endosomal-recycling",totalDownloads:1342,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Peripheral membrane proteins are endocytosed by constitutive processes of membrane invaginations, followed by internalization driven by diverse endocytic machinery available at the cell surface. It is believed that after endocytic uptake, cargo proteins proceed either through the endosomal recycling circuit of the cell or travel toward late endosomes for degradation. In this chapter, we analyzed trafficking of seven cargo molecules (transferrin receptor, fully conformed MHC-I, non-conformed MHC-I, cholera-toxin B subunit, CD44, ICAM1, and G-protein-coupled receptor Rae-1) known to use the distinct endocytic route. For that purpose, we developed the software for multicompartment analysis of intracellular trafficking. We demonstrate that all endocytosed molecules are rapidly recycled and propose that the rapid recycling is a constitutive process that should be considered in the analysis of intracellular trafficking of peripheral membrane proteins.",book:{id:"6649",slug:"peripheral-membrane-proteins",title:"Peripheral Membrane Proteins",fullTitle:"Peripheral Membrane Proteins"},signatures:"Hana Mahmutefendić, Gordana Blagojević Zagorac, Senka Maćešić\nand Pero Lučin",authors:[{id:"152008",title:"Prof.",name:"Pero",middleName:null,surname:"Lučin",slug:"pero-lucin",fullName:"Pero Lučin"},{id:"245873",title:"Prof.",name:"Hana",middleName:null,surname:"Mahmutefendić",slug:"hana-mahmutefendic",fullName:"Hana Mahmutefendić"},{id:"245875",title:"Prof.",name:"Gordana",middleName:null,surname:"Blagojević Zagorac",slug:"gordana-blagojevic-zagorac",fullName:"Gordana Blagojević Zagorac"},{id:"245876",title:"Prof.",name:"Senka",middleName:null,surname:"Maćešić",slug:"senka-macesic",fullName:"Senka Maćešić"}]}],onlineFirstChaptersFilter:{topicId:"913",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:32,numberOfPublishedChapters:318,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:15,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}}]},series:{item:{id:"14",title:"Artificial Intelligence",doi:"10.5772/intechopen.79920",issn:"2633-1403",scope:"Artificial Intelligence (AI) is a rapidly developing multidisciplinary research area that aims to solve increasingly complex problems. In today's highly integrated world, AI promises to become a robust and powerful means for obtaining solutions to previously unsolvable problems. This Series is intended for researchers and students alike interested in this fascinating field and its many applications.",coverUrl:"https://cdn.intechopen.com/series/covers/14.jpg",latestPublicationDate:"June 11th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:9,editor:{id:"218714",title:"Prof.",name:"Andries",middleName:null,surname:"Engelbrecht",slug:"andries-engelbrecht",fullName:"Andries Engelbrecht",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRNR8QAO/Profile_Picture_1622640468300",biography:"Andries Engelbrecht received the Masters and PhD degrees in Computer Science from the University of Stellenbosch, South Africa, in 1994 and 1999 respectively. He is currently appointed as the Voigt Chair in Data Science in the Department of Industrial Engineering, with a joint appointment as Professor in the Computer Science Division, Stellenbosch University. Prior to his appointment at Stellenbosch University, he has been at the University of Pretoria, Department of Computer Science (1998-2018), where he was appointed as South Africa Research Chair in Artifical Intelligence (2007-2018), the head of the Department of Computer Science (2008-2017), and Director of the Institute for Big Data and Data Science (2017-2018). In addition to a number of research articles, he has written two books, Computational Intelligence: An Introduction and Fundamentals of Computational Swarm Intelligence.",institutionString:null,institution:{name:"Stellenbosch University",institutionURL:null,country:{name:"South Africa"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:6,paginationItems:[{id:"22",title:"Applied Intelligence",coverUrl:"https://cdn.intechopen.com/series_topics/covers/22.jpg",isOpenForSubmission:!0,editor:{id:"27170",title:"Prof.",name:"Carlos",middleName:"M.",surname:"Travieso-Gonzalez",slug:"carlos-travieso-gonzalez",fullName:"Carlos Travieso-Gonzalez",profilePictureURL:"https://mts.intechopen.com/storage/users/27170/images/system/27170.jpeg",biography:"Carlos M. Travieso-González received his MSc degree in Telecommunication Engineering at Polytechnic University of Catalonia (UPC), Spain in 1997, and his Ph.D. degree in 2002 at the University of Las Palmas de Gran Canaria (ULPGC-Spain). He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. He is the founder of The IEEE IWOBI conference series and the president of its Steering Committee, as well as the founder of both the InnoEducaTIC and APPIS conference series. He is an evaluator of project proposals for the European Union (H2020), Medical Research Council (MRC, UK), Spanish Government (ANECA, Spain), Research National Agency (ANR, France), DAAD (Germany), Argentinian Government, and the Colombian Institutions. He has been a reviewer in different indexed international journals (<70) and conferences (<250) since 2001. He has been a member of the IASTED Technical Committee on Image Processing from 2007 and a member of the IASTED Technical Committee on Artificial Intelligence and Expert Systems from 2011. \n\nHe has held the general chair position for the following: ACM-APPIS (2020, 2021), IEEE-IWOBI (2019, 2020 and 2020), A PPIS (2018, 2019), IEEE-IWOBI (2014, 2015, 2017, 2018), InnoEducaTIC (2014, 2017), IEEE-INES (2013), NoLISP (2011), JRBP (2012), and IEEE-ICCST (2005)\n\nHe is an associate editor of the Computational Intelligence and Neuroscience Journal (Hindawi – Q2 JCR-ISI). He was vice dean from 2004 to 2010 in the Higher Technical School of Telecommunication Engineers at ULPGC and the vice dean of Graduate and Postgraduate Studies from March 2013 to November 2017. He won the “Catedra Telefonica” Awards in Modality of Knowledge Transfer, 2017, 2018, and 2019 editions, and awards in Modality of COVID Research in 2020.\n\nPublic References:\nResearcher ID http://www.researcherid.com/rid/N-5967-2014\nORCID https://orcid.org/0000-0002-4621-2768 \nScopus Author ID https://www.scopus.com/authid/detail.uri?authorId=6602376272\nScholar Google https://scholar.google.es/citations?user=G1ks9nIAAAAJ&hl=en \nResearchGate https://www.researchgate.net/profile/Carlos_Travieso",institutionString:null,institution:{name:"University of Las Palmas de Gran Canaria",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"23",title:"Computational Neuroscience",coverUrl:"https://cdn.intechopen.com/series_topics/covers/23.jpg",isOpenForSubmission:!0,editor:{id:"14004",title:"Dr.",name:"Magnus",middleName:null,surname:"Johnsson",slug:"magnus-johnsson",fullName:"Magnus Johnsson",profilePictureURL:"https://mts.intechopen.com/storage/users/14004/images/system/14004.png",biography:"Dr Magnus Johnsson is a cross-disciplinary scientist, lecturer, scientific editor and AI/machine learning consultant from Sweden. \n\nHe is currently at Malmö University in Sweden, but also held positions at Lund University in Sweden and at Moscow Engineering Physics Institute. \nHe holds editorial positions at several international scientific journals and has served as a scientific editor for books and special journal issues. \nHis research interests are wide and include, but are not limited to, autonomous systems, computer modeling, artificial neural networks, artificial intelligence, cognitive neuroscience, cognitive robotics, cognitive architectures, cognitive aids and the philosophy of mind. \n\nDr. Johnsson has experience from working in the industry and he has a keen interest in the application of neural networks and artificial intelligence to fields like industry, finance, and medicine. \n\nWeb page: www.magnusjohnsson.se",institutionString:null,institution:{name:"Malmö University",institutionURL:null,country:{name:"Sweden"}}},editorTwo:null,editorThree:null},{id:"24",title:"Computer Vision",coverUrl:"https://cdn.intechopen.com/series_topics/covers/24.jpg",isOpenForSubmission:!0,editor:{id:"294154",title:"Prof.",name:"George",middleName:null,surname:"Papakostas",slug:"george-papakostas",fullName:"George Papakostas",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002hYaGbQAK/Profile_Picture_1624519712088",biography:"George A. Papakostas has received a diploma in Electrical and Computer Engineering in 1999 and the M.Sc. and Ph.D. degrees in Electrical and Computer Engineering in 2002 and 2007, respectively, from the Democritus University of Thrace (DUTH), Greece. Dr. Papakostas serves as a Tenured Full Professor at the Department of Computer Science, International Hellenic University, Greece. Dr. Papakostas has 10 years of experience in large-scale systems design as a senior software engineer and technical manager, and 20 years of research experience in the field of Artificial Intelligence. Currently, he is the Head of the “Visual Computing” division of HUman-MAchines INteraction Laboratory (HUMAIN-Lab) and the Director of the MPhil program “Advanced Technologies in Informatics and Computers” hosted by the Department of Computer Science, International Hellenic University. He has (co)authored more than 150 publications in indexed journals, international conferences and book chapters, 1 book (in Greek), 3 edited books, and 5 journal special issues. His publications have more than 2100 citations with h-index 27 (GoogleScholar). His research interests include computer/machine vision, machine learning, pattern recognition, computational intelligence. \nDr. Papakostas served as a reviewer in numerous journals, as a program\ncommittee member in international conferences and he is a member of the IAENG, MIR Labs, EUCogIII, INSTICC and the Technical Chamber of Greece (TEE).",institutionString:null,institution:{name:"International Hellenic University",institutionURL:null,country:{name:"Greece"}}},editorTwo:null,editorThree:null},{id:"25",title:"Evolutionary Computation",coverUrl:"https://cdn.intechopen.com/series_topics/covers/25.jpg",isOpenForSubmission:!0,editor:{id:"136112",title:"Dr.",name:"Sebastian",middleName:null,surname:"Ventura Soto",slug:"sebastian-ventura-soto",fullName:"Sebastian Ventura Soto",profilePictureURL:"https://mts.intechopen.com/storage/users/136112/images/system/136112.png",biography:"Sebastian Ventura is a Spanish researcher, a full professor with the Department of Computer Science and Numerical Analysis, University of Córdoba. Dr Ventura also holds the positions of Affiliated Professor at Virginia Commonwealth University (Richmond, USA) and Distinguished Adjunct Professor at King Abdulaziz University (Jeddah, Saudi Arabia). Additionally, he is deputy director of the Andalusian Research Institute in Data Science and Computational Intelligence (DaSCI) and heads the Knowledge Discovery and Intelligent Systems Research Laboratory. He has published more than ten books and over 300 articles in journals and scientific conferences. Currently, his work has received over 18,000 citations according to Google Scholar, including more than 2200 citations in 2020. In the last five years, he has published more than 60 papers in international journals indexed in the JCR (around 70% of them belonging to first quartile journals) and he has edited some Springer books “Supervised Descriptive Pattern Mining” (2018), “Multiple Instance Learning - Foundations and Algorithms” (2016), and “Pattern Mining with Evolutionary Algorithms” (2016). He has also been involved in more than 20 research projects supported by the Spanish and Andalusian governments and the European Union. He currently belongs to the editorial board of PeerJ Computer Science, Information Fusion and Engineering Applications of Artificial Intelligence journals, being also associate editor of Applied Computational Intelligence and Soft Computing and IEEE Transactions on Cybernetics. Finally, he is editor-in-chief of Progress in Artificial Intelligence. He is a Senior Member of the IEEE Computer, the IEEE Computational Intelligence, and the IEEE Systems, Man, and Cybernetics Societies, and the Association of Computing Machinery (ACM). Finally, his main research interests include data science, computational intelligence, and their applications.",institutionString:null,institution:{name:"University of Córdoba",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"26",title:"Machine Learning and Data Mining",coverUrl:"https://cdn.intechopen.com/series_topics/covers/26.jpg",isOpenForSubmission:!0,editor:{id:"24555",title:"Dr.",name:"Marco Antonio",middleName:null,surname:"Aceves Fernandez",slug:"marco-antonio-aceves-fernandez",fullName:"Marco Antonio Aceves Fernandez",profilePictureURL:"https://mts.intechopen.com/storage/users/24555/images/system/24555.jpg",biography:"Dr. Marco Antonio Aceves Fernandez obtained his B.Sc. (Eng.) in Telematics from the Universidad de Colima, Mexico. He obtained both his M.Sc. and Ph.D. from the University of Liverpool, England, in the field of Intelligent Systems. He is a full professor at the Universidad Autonoma de Queretaro, Mexico, and a member of the National System of Researchers (SNI) since 2009. Dr. Aceves Fernandez has published more than 80 research papers as well as a number of book chapters and congress papers. He has contributed in more than 20 funded research projects, both academic and industrial, in the area of artificial intelligence, ranging from environmental, biomedical, automotive, aviation, consumer, and robotics to other applications. He is also a honorary president at the National Association of Embedded Systems (AMESE), a senior member of the IEEE, and a board member of many institutions. 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Dr. Aydin is currently a Fellow of Higher Education Academy, UK, a member of EPSRC College, a senior member of IEEE and a senior member of ACM. In addition to being a member of advisory committees of many international conferences, he is an Editorial Board Member of various peer-reviewed international journals. 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