bluuebunny/crossref_metadata_2025 huggingface dataset:
Lyme Disease
Authors: Belman Anita L. , Preston Thomas
Published: November 2020

Lyme disease (LD), caused by the arthropod-borne spirochete Borrelia burgdorferi, is a multisystem disease of varying severity. Since its recognition as a distinct clinical entity in 1977 (Steere et al. 1977), recovery of the causative organism from the tick vector in 1982 (Barbour 1984; Burgdorfer et al. 1982), and isolation of the organism from patients in 1983 (Benach et al. 1983), LD, also referred to as Lyme borreliosis, has emerged as the leading vector-transmitted disease in the United States (CDC 2007). Lyme disease became a concern especially for children residing in endemic areas. Initially described as a rheumatologic illness (inflammatory arthritis, predominantly in children), it soon became clear that LD is a multisystem disease (Steere 1989; Feder 2008; Halperin 2008; Hoppa 2007; Hytnen et al. 2008; Pachner and Steiner 2007; Steere et al. 1984). Neurologic involvement is common and can add significantly to the morbidity of the illness. A wide range of neurologic complications has been described (Belman 1992; Belman et al. 1992, 1993; Christen and Hanefield 1993; Christen et al. 1993; Coyle 1992; Halperin et al. 1989, 1990; Logigian, Kaplan, and Steere 1990; Logigian and Steere 1992; Pachner and Steeere 1986; Pachner, Duray, and Steere 1989; Reik et al. 1979; Reik, Burgdorfer, and Donaldson 1986). Borrelia burgdorferi (Bb) is a motile, helicial Gram-negative spirochete containing both chromosomal DNA and extra chromosomal double-stranded DNA. Both chromosomal and plasmid DNA code for proteins. Some proteins are constant major proteins, common to spirochetes in general, and some are proteins unique and specific to B. burgdoerferi, for example, the plasmidcoded outer surface lipoproteins (OSP). These specific and nonspecific proteins (antigens) form the basis for serological antibody tests (presence or absence of specific anti-Bb antibodies against Bb antigens) (CDC 1995; Dressler 1994). The OSPs play a role in the pathogenesis of Bb infection by acting as receptors for host macromolecules and targets for host immune response (Tilly, Rosa, and Stewart. 2008). Several B. burgdoerferi species have been identified, with varying geographic distribution. Different species may have different tissue tropism and pathogenecity and cause different clinical disease patterns (Anthonissen et al. 1994; Piesman and Gern 2004; Stanek and Strle 2008).
Neurological and Cognitive Consequences of Nephropathic Cystinosis
Authors: Trauner Doris A.
Published: November 2020

Nephropathic cystinosis is a rare autosomal recessive disorder caused by a deletion mapped to chromosome 17p13. The gene codes for a protein, cystinosin (CTNS), a lysosomal membrane transporter protein. When the CTNS gene is inactivated, the amino acid cystine cannot cross the lysosomal membrane and accumulates in lysosomes. Thus, cystinosis is a lysosomal storage disease. The accumulated cystine forms crystals that can cause damage to multiple organs. Cystinosis is thought to occur with an incidence of 1 in 100,000 live births, although accurate numbers are difficult to obtain because the disease may remain undiagnosed. Cystinosis was first described as a renal tubular disorder in the early 20th century by Fanconi and others (see Gahl et al. 2002 for a review). In 1967, accumulation of cystine within cells was recognized, and the lysosomal transport defect was identified in 1982. The first signs and symptoms of cystinosis are caused by renal tubular dysfunction, with the Fanconi syndrome developing within the first few months of life. Infants develop polyuria, dehydration, vomiting, poor appetite, and excessive thirst. If not recognized and treated early, these infants have failure to thrive and may develop rickets. The diagnosis can be made by assaying the cystine concentration in white blood cells; a level of greater than 2 nmol half-cystine per milligram of protein is diagnostic. The gene can now be sequenced, but this is conducted primarily in research settings and is not readily available clinically. Once diagnosed, treatment with a cystine-depleting agent, cysteamine, can be introduced immediately. The natural history of untreated nephropathic cystinosis is that of progressive renal failure, with renal dialysis and ultimately kidney transplant typically being necessary by the age of 10 years. Even with successful renal transplantation, life expectancy is greatly shortened, with death typically in the third or fourth decade. The reason for the early mortality is that cystinosis affects multiple other organs besides the kidney, and renal transplantation does not prevent the other systemic complications. Although the most prominent manifestations of the disease are renal, other organs are involved to varying degrees.
Phenylketonuria
Authors: Brumm Virdette L.
Published: November 2020

Phenylketonuria (PKU) is the most frequent disorder of amino acid metabolism. First described by Fölling in 1934, PKU is an autosomal recessive disorder involving mutations in the phenylalanine hydroxylase (PAH) gene, which inhibits the normal metabolism of phenylalanine, an amino acid found in all proteins (Scriver et al. 2001). As a result, phenylalanine cannot be converted into tyrosine and accumulates in the blood and other tissues in untreated patients on a normal diet (Huijbregts et al. 2003; Pietz et al. 1998). The degree of impairment varies significantly among patients, resulting in a broad continuum of phenotypes (NIH Consensus Development Conference Report 2001). Phenylketonuria is the most common biochemical cause of mental retardation (Scriver et al. 1995). When untreated, increased phenylalanine concentrations in blood and tissues and low to normal tyrosine concentrations result in severe mental and neurological retardation (Scriver et al. 1995). In 1953, a treatment was discovered by Horst Bickel and his colleagues in England (Bickel et al. 1953). The treatment has become a standard of care and is based on a phenylalanine-restricted diet that consists of severe restriction of natural protein supplemented with all amino acids, except phenylalanine, to compensate for the shortage of amino acids through regular protein intake (Huijbregts et al. 2003). The work of Bickel and his colleagues proved that excessive phenylalanine resulted in neurological problems and that dietary treatment was beneficial. Patients with both classical and less severe forms of PKU require dietary protein restriction to prevent neurological sequelae and to ensure normal cognitive development. The first newborn screening program began in 1961 and initial results were reported by Guthrie and Susi (1963). The Guthrie bacterial assay for the filter paper blood test made it possible to identify PKU from a drop of blood from the heel of a newborn within the first days of life. It was then possible to begin treatment and thereby prevent mental retardation. Today, laws mandating newborn screening are in place in North American and Europe.
Neurocognitive Effects of Solid Organ Transplantation
Authors: Zelikovsky Nataliya , Lefkowitz Debra S.
Published: November 2020

The first successful organ transplant was a kidney transplant performed between identical twins in 1954. Since that time, major medical advances have been made to help improve survival rates for transplant recipients. In 2008, there were 1,964 solid organ transplants performed for children under age 18 (2007 Organ Procurement and Transplantation Network and the Scientific Registry of Transplant Recipients [OPTN/SRTR] Annual Report 1997–2006). Currently, approximately 1,830 pediatric patients are awaiting some type of solid organ transplant (2007 OPTN/SRTR Annual Report 1997–2006). Organ transplantation in children is relatively recent compared to other treatments for children with chronic illnesses. The focus over the first few decades has been on medical advances and improving survival rates for transplant patients. In the recent years, increasing attention has been given to the developmental, neurocognitive, and psychosocial outcomes prior to transplant and in the short-term period post transplant. Most chronic illnesses and acute traumatic medical events have implications for neurocognitive outcomes. End-stage disease of the liver, kidney, heart, and lung are all believed to affect intellectual, academic, and neurocognitive functions. Gross neurodevelopmental deficits have become less common due to early medical intervention (e.g., improved nutrition, surgical intervention, reduced exposure to aluminum (Warady 2002). Organ transplantation is believed to ameliorate the deleterious long-term developmental and neurocognitive effects, but this topic has received little attention in the literature, and the available results with regard to intellectual, academic, and neurodevelopmental results have been mixed. In a combined sample of solid organ transplant patients, 40% had clinically significant cognitive delays (Brosig et al. 2006). Examining the impact of different underlying disease processes and transplantation of each solid organ separately is critical. Thus, we discuss the neurocognitive outcomes of each organ group separately in this chapter. Neurocognitive outcomes can be assessed in a variety of ways depending upon the age of the child. Among infants and toddlers, neurocognitive functioning is measured by an assessment of motor function, social and environmental interaction, and language development. Assessment of older children may involve the evaluation of intelligence, academic achievement, emotional and behavioral functioning, and adaptive skills.
Asthma and Cystic Fibrosis
Authors: Hilt Robert , Leary Alison
Published: November 2020

Asthma and cystic fibrosis (CF) are examples of childhood pulmonary illnesses with significant psychological impacts. These disorders have in common an induced difficulty with a primal drive, the drive to breathe. Acute impairment with the drive to breathe is highly anxiety provoking, and chronic impairment is life-altering. Pulmonary illnesses like asthma and CF can have direct impacts on brain functioning through systemic hypoxia (low blood oxygen [O2] level) or hypercapnia (high blood carbon dioxide [CO2] level) due to poor respiratory gas exchange. With chronic respiratory problems in children, hypoxia is the more clinically pertinent issue in that hypoxia seems to produce developmental impacts. Studies that have looked at the outcomes of pulmonary hypoxia have found associations with adverse effects even from oxygen levels that were just slightly below the normal range (Bass et al. 2004). A drop of only 4% O2 saturation from baseline is associated with attentiondeficit hyperactivity (ADHD)-like symptoms. Persistent oxygen saturation levels that are even lower than this have been associated with decreased IQ and delays in motor development (Bass et al. 2004). Negative neurobehavioral effects of the hypercapnia side of impaired respiratory status are less well documented. In fact, hypercapnia, besides triggering an increase in cerebral blood flow and driving a sense of air hunger particularly in people with trait anxiety, seems to have no lasting neurocognitive impact (Wan et al. 2008). Research on the use of intentional ‘‘permissive’’ hypercapnia when using mechanical ventilation assistance (allowing higher blood carbon dioxide levels to minimize barotrauma from the assist device) has shown no common neurocognitive complications from this strategy. There are even suggestions of some improved neurocognitive outcomes for neonates managed in this manner (Miller and Carlo 2007). These results are tempered by a higher reported frequency of intraventricular hemorrhage in hypercapnic very-low-birth-weight infants, and there is at least one case report of subarachnoid hemorrhage in a child ventilated with permissive hypercapnia for an asthma episode (Edmunds and Harrison 2003; Kaiser et al. 2006). The severe hypercapnia of complete respiratory failure goes hand in hand with hypoxia, so the effects of each in that potentially fatal scenario are difficult to separate.
The Behavioral and Cognitive Manifestations of Blindness in Children
Authors: Pring Linda , Tadić Valerie
Published: November 2020

Ground-breaking progress in the field of neurodevelopmental disorders has allowed us far more insight into blindness and visual impairment (VI). The field of cognitive neuroscience has now established itself solidly in the literature, combining the knowledge from cognitive psychology, clinical studies related to brain damage, and neuroscience to open the way to significant advances in understanding. In recent years, the optimism engendered from the adult studies has played a large part in providing the impetus for developmental studies and in particular developmental neuroscience (Johnson 2005; Tager-Flusberg 1999). It is from this developmental neuroscience perspective that we can begin to understand the cognitive and behavioral manifestations associated with blindness and VI; albeit with the proviso that children with VI present particularly heterogeneous developmental patterns when compared to typically developing children (Fraiberg 1971). In considering the effects of blindness and VI, this chapter will focus on social understanding, language, cognition, and motor development. However, it begins with brief introductions to epidemiology and the effects of blindness on the functional and structural organization of the brain, which it is hoped will provide a useful context in which to consider the development of children who cannot see. Today the number of blind people in the world stands at 45 million, even though up to 75% of blindness could be avoided either by treatment or by prevention. The number of people with avoidable blindness will have doubled from 1990 to 2020 unless there is rapid and effective intervention, and the total number of the blind is projected to be as many as 76 million by 2020. To prevent this scenario, the World Health Organization (WHO) and the International Agency for the Prevention of Blindness (IAPB) have jointly initiated Vision 2020, a project that aims to eliminate the main causes of avoidable blindness by the year 2020, with the ultimate long-term goal of a world in which all avoidable blindness is eliminated and in which everyone with unavoidable vision loss reaches their full potential. The top priority of Vision 2020 is the prevention of childhood blindness. At present there are 1.4 million children under the age of 15 who are blind.
Fetal Alcohol Spectrum Disorders
Authors: Thorne John C. , Jirikowic Tracy
Published: November 2020

Fetal alcohol spectrum disorders (FASD) is an umbrella term used to refer to the range of negative outcomes associated with prenatal ethyl-alcohol exposure (PAE). Although the impact of maternal drinking on the pre and postnatal development of children was examined as early as the late 19th century (Sullivan 1899), the teratogenic effects of PAE were not widely recognized until 1973, when Jones and Smith discussed PAE. The fetal alcohol syndrome (FAS) they described is now recognized internationally as a permanent birth defect syndrome resulting from PAE. Fetal alcohol syndrome is characterized by growth deficiency, a unique cluster of three minor facial anomalies, and evidence of central nervous system (CNS) abnormalities. At an estimated prevalence of one to three cases per 1,000 live births, FAS is the leading known preventable cause of developmental and intellectual disabilities (Bailey and Sokol 2008). Because the distinctive FAS facial phenotype provides a specific diagnostic marker of PAE (Astley 2006), FAS is the most readily recognized of the FASD. Fetal alcohol spectrum disorders that lack the tell-tale facial phenotype of FAS are more difficult to diagnose, but share a similar range and severity of CNS impairments and social costs. Other FASDs are many times more prevalent than FAS (Bailey and Sokol 2008) and may occur in as many as 1% of all children. Along with CNS, craniofacial, and growth impairments, FASD may also include ophthalmologic, cardiac, renal, and orthopedic abnormalities. Although heavier PAE, particularly binge drinking, leads to increased risk of FASD, no safe exposure level has been established. It is apparent that risk is substantially increased if the mother is older, has a history of alcoholism, has a family history of FASD, or is living in poverty. However, no clear set of risk or protective factors has been determined for any FASD that would allow for evidence-based advice to a particular mother on the relative risk that a particular level of drinking might have on her child’s development (Bailey and Sokol 2008; Jacobson et al. 2004; Maier and West 2001; Nulman et al. 2004; see also Disney et al. 2008).
Cognitive and Behavioral Manifestations of Lead
Authors: Evans Hugh L.
Published: November 2020

The link between exposure to lead and children’s cognitive problems was implied in the earliest medical reports of frank lead poisoning of young children in Australia in the 1800s (Lin-Fu 1992). Children with acute severe toxicity of lead (Pb) are now rarely seen in the United States. However, millions of children may have subclinical neurobehavioral disorders associated with chronic low-level exposure to lead, representing a major public health concern (Bellinger 2008a). Lead is a nonessential metal that is recognized as a source of toxic exposure, with the developing nervous system particularly vulnerable. Because of this, U.S. regulations limiting the lead content of gasoline and household paint have led to a gradual reduction of the average blood lead concentration of Americans over the last three decades. Average blood lead levels of children in the United States dropped an estimated 78% from 1976 to 1991 (Brody et al. 1994; Caldwell et al. 2009). Despite these reductions in exposure to lead, new advances in research techniques have documented harmful consequences associated with lower blood lead levels. This raises the possibility that there is no threshold for occurrence of lead-induced toxicity. Bellinger (2008a) refers to “the silent pandemic of neurodevelopmental disorders resulting from children’s continuing exposure to low levels of lead.” The developing brain may be more sensitive to exposure to lead than the adult. Since the pioneering work of Needleman and colleagues (1979), a large scientific literature has documented the deleterious effects of pre- and neonatal exposure to lead. Decrements in IQ scores have proven to be among the most sensitive and consistent consequences of a child’s exposure to lead, but other cognitive and behavioral changes have been described as well, including attention-deficit hyperactivity disorder (ADHD). Among the important current sources of children’s exposure to lead is household dust (Dixon et al. 2009) the lead content in old water pipes, batteries, and from contamination by numerous industrial processes. Pre and postnatal exposure to cigarette smoke is a cofactor with lead exposure in children’s conduct disorders (Braun et al. 2008). Diagnosis of lead-induced disorders involves the determination of exposure to lead and the atomic absorption assay of lead in whole blood.
Cognitive Complications of Mercury Exposure
Authors: Evans Hugh L.
Published: November 2020

Mercury (Hg) is a nonessential metal that has been used in a variety of industrial procedures and pharmaceutical preparations over centuries, resulting in hot spots of environmental contamination and unwanted toxicity in people who were occupationally exposed or were treated with mercury compounds (Clarkson and Magos 2006; Evans 1998). Mercury exists in three different chemical forms, each having a different profile of toxicity. The central nervous system (CNS) is considered to be the target organ for organic mercury and elemental mercury. The kidneys are considered to be the target organ of inorganic mercury. The most widespread current exposure of children is to organic mercury from ingestion of seafood, most of which is in the form of methylmercury, the most severely neurotoxic form of mercury (Clarkson and Magos 2006). Maternal consumption of seafood, although nutritionally beneficial, has been associated with elevated mercury levels in maternal blood and hair, and with deleterious outcomes in their infants. Mothers can transit mercury to their fetus through their blood supply or to their infant through maternal milk. Children also are exposed to mercury in regions where gold is mined (Bose-O’Reilly et al. 2008). Other sources of exposures have been reviewed by Clarkson and Magos (2006). Over the past two decades in the United States, mercury has been increasingly restricted by the U.S. Environmental Protection Agency, and it has been removed from consumer products (where it had been used as a fungicide). Current efforts are under way to encourage consumers to trade their mercury thermometers for newer models that do not use mercury. Mercury has no essential nutritional role, so any amount of mercury in the body can be considered undesirable. For practical purposes, since mercury is present at some level almost everywhere on Earth, the key question is at what dose or concentration in the body can mercury-induced toxicity be documented? Continuing improvements in chemical measurement has resulted in the determining of mercury in lower concentrations. This has been matched by advances in neurological measurements and statistical analyses, resulting in the extrapolation of lower “safe” levels of mercury levels in drinking water, hair, and blood.
What Is Electroconvulsive Therapy?
Authors: Fink MD Max
Published: November 2020

Electroconvulsive therapy (ECT) is an effective medical treatment for severe and persistent psychiatric disorders. It relieves de pressed mood and thoughts of suicide, as well as mania, acute psychosis, delirium, and stupor. It is usually applied when medications have given limited relief or their side effects are intolerable. Electroconvulsive therapy is similar to a surgical treatment. It requires the specialized skills of a psychiatrist, an anesthesiologist, and nurses. The patient receives a short-acting anesthetic. While the patient is asleep, the physician, following a prescribed procedure, induces an epileptic seizure in the brain. By making sure that the patient’s lungs are filled with oxygen, the physician precludes the gasping and difficult breathing that accompany a spontaneous epileptic fit. By relaxing the patient’s muscles with chemicals and by inserting a mouth guard (not unlike those used in sports), the physician prevents the tongue biting, fractures, and injuries that occasionally occur in epilepsy. The patient is asleep, and so experiences neither the painful effects of the stimulus nor the discomforts of the seizure. The physiological functions of the body, such as breathing, heart rate, blood pressure, blood oxygen concentration, and degree of motor relaxation, are monitored, and anything out of the ordinary is immediately treated. Electroconvulsive therapy relieves symptoms more quickly than do psychotropic drugs. A common course of ECT consists of two or three treatments a week for two to seven weeks. To sustain the recovery, weekly or biweekly continuation treatments, either ECT or medications, are often administered for four to six months. If the illness recurs, ECT is prescribed for longer periods. The duration and course of ECT are similar to those of the psychotropic medicines frequently used for the same conditions. Electroconvulsive therapy has been used safely to treat emotional disorders in patients of all ages, from children to the elderly, in people with debilitating physical illnesses, and in pregnant women. Emotional disorders may be of short or long duration; they may be manifest as a single episode or as a recurring event. Electroconvulsive treatment is an option when the emotional disorder is acute in onset; when changes in mood, thought, and motor activities are pronounced; when the cause is believed to be biochemical or physiological; when the condition is so severe that it interferes with the patient’s daily life; or when other treatments have failed.
Learning to Write Like a Chemist
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

Chapter 1 introduces the basic approach to reading and writing in chemistry used in this textbook. It also provides a brief orientation to the textbook. By the end of this chapter, you should be able to do the following: ■ Identify common writing genres in chemistry and in this textbook ■ Describe the five essential components of genre analysis and explain why genre analysis is so useful for developing writers ■ Explain what is meant by audience, and identify the audiences addressed in this textbook ■ Differentiate between broad and fine organizational structure ■ Explain the meaning and significance of a move and a move structure ■ Understand how the textbook is organized and the approach it takes to help you improve your chemistry writing skills Many effective writers develop their discipline-specific writing skills by reading and analyzing the works of others in their fields. Learning to write in chemistry is no exception; chemistry-specific writing skills are developed by reading and analyzing the writing of chemists. We coined the phrase “read-analyze-write” to describe this approach and promote this process throughout the textbook. In this chapter, we lay the foundation for the read-analyze-write approach by analyzing a few common, nonscientific examples of writing. We use these everyday examples (e.g., letters, recipes, jokes, used-car ads, poems) to introduce you to the process of analyzing writing and to share with you the tools that you will need to analyze chemistry writing in subsequent chapters.
Writing the Discussion Section
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

This chapter focuses on the Discussion section, the last part of the standard IMRD structure for a journal article. The Discussion section, as mentioned in chapter 4, can stand alone or can be part of a combined Results and Discussion (R&D) section. In either case, it serves the same major purpose: to interpret the results of the study. In this chapter, we analyze excerpts from various Discussion sections, including those that accompany results presented in chapter 4 (excerpts 4B–4G). Upon completion of this chapter, you should be able to do the following: ■ Organize a Discussion section following the major moves ■ Interpret your results (but avoid overinterpretation) ■ Describe the greater importance of your findings ■ Follow appropriate writing conventions As you work through this chapter, you will write a Discussion section for your own paper. The Writing on Your Own tasks throughout the chapter will guide you step by step as you do the following: 5A Read the literature 5B Prepare to write 5C Draft your Discussion section 5D Practice peer review 5E Fine-tune your Discussion section In the Discussion section of a journal article, authors interpret their data, address why and how questions (e.g., Why was the reaction faster? How did the mechanism proceed?), and, ultimately, extend their findings to a larger context (e.g., What value will these findings have to the scientific community?). Ideally, the Discussion section explains the story revealed by the data, postulates reasons for the observed behaviors, and furthers our fundamental understanding of the underlying science. Although interpretation is the primary goal of the Discussion section, authors must be careful not to overinterpret their data, misinterpret their results, overstate their assumptions, or stray too far from scientific evidence. The excerpts selected for this chapter illustrate ways to avoid these pitfalls. Similarly, the excerpts illustrate that the language of the Discussion section is typified by restraint and understatement. Such words as fact, truth, and prove are rarely used in a Discussion section. Hedging words, such as theory and evidence, are much more common, as are such verbs as appear, indicate, seem, and suggest.
Writing the Poster Text
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

Congratulations! If you are reading this chapter, you are likely preparing a poster for a scientific conference. This means that your conference abstract was accepted and that you have been invited to give a poster presentation. In this chapter, we focus on the various sections of the poster and how to write them. In chapter 10, we highlight the visual attributes of the poster (layout, font size, color schemes, etc.). By the end of this chapter, you will be able to do the following: ■ Address the correct audience in your poster ■ Write the major sections of your poster ■ Use bulleted lists and graphics appropriately ■ Add title, references, and acknowledgments to your poster As you work through the chapter, you will compose the text and graphics for your own poster. The Writing on Your Own tasks throughout this chapter guide you step by step as you do the following: 9A Prepare to write 9B Draft your poster Methods section 9C Draft your poster Results section 9D Draft your poster Discussion section 9E Draft your poster Introduction section 9F Add your poster title, author list, acknowledgments, and references We begin by asking you to read and analyze a poster that we created based on the journal article by Vesely et al. (2003) regarding aldehydes in beer. Journal articles usually include far too much information for a single poster; hence, in the poster in figure 9.1, we include only a fraction of the information presented in the full journal article. (For the full article, see excerpts 3A, 4A, 6A, and 7A.) The hypothetical poster focuses on what Vesely’s group might have presented early in their research project, specifically, the methods that they developed to analyze their samples. A black-and-white version of the poster is presented in figure 9.1; a full-color version of the poster is available on the Write Like a Chemist Web site. Exercise 9.1 guides you in the analysis of the poster and lays the groundwork for the rest of the chapter.
Writing the Goals and Importance Section
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

This chapter focuses on writing the first section of the Project Description. The central purposes of this section are to identify project goals and objectives, highlight the importance of the research, provide relevant background information, and introduce the proposed research. By the end of this chapter, you should be able to do the following: ■ Distinguish between broad goals and specific objectives ■ Format a list of objectives correctly ■ Emphasize the importance of your research ■ Affirm your intellectual merit ■ Know when and how to introduce your proposed work ■ Select appropriate headings As you work through the chapter, you will write the opening section of your Project Description. The Writing on Your Own tasks throughout the chapter guide you step by step as you do the following: 12A Prepare to write 12B Create a list of project goals and objectives 12C Introduce and develop the research story 12D Introduce your proposed work 12E Complete the opening section We begin with excerpt 12A for you to read and analyze on your own. The excerpt contains only parts of the author’s original Goals and Importance section. Her full section starts with a statement of goals and significance, which is followed by individual descriptions of three separate but related studies. In excerpt 12A, we include only (1) the statement of goals and significance and (2) the description of the second study.
Writing the Project Summary and Title
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

The Project Summary is a short description of the proposed work (one page or less), which, unlike the rest of the proposal, can be accessed by the public. It is usually the first page of the proposal (excluding the cover page, which provides institutional information) and, therefore, precedes the Project Description. In this chapter, we consider the Project Summary and highlight a few language features pertinent to the summary. We conclude the chapter (and module) with suggestions for writing a title for your proposal. By the end of this chapter, you will be able to do the following: ■ Recognize the audience and purpose for the Project Summary ■ Know what content should be included in (and excluded from) the Project Summary ■ Follow the typical move structure of the Project Summary ■ Write an appropriate title for your proposal As you work through the chapter, you will write your Project Summary and give your proposal a title. The Writing on Your Own tasks throughout the chapter will guide you step by step as you do the following: 15A Write the Project Summary 15B Write the proposal title 15C Complete the proposal Most external funding agencies require a Project Summary. Funding agencies often share project summaries with their donors, boards of directors, prospective grantees, and others interested in the types of projects that they fund. The Project Summary is also used by program officers to determine the most appropriate review panel for the proposal. In complex agencies like the NSF and NIH, there are many related program initiatives, and it is ultimately the decision of the program officer to forward the proposal to the right division for consideration. As such, the Project Summary is typically written for a scientific audience, enabling a scientifically literate but nonexpert audience to understand the project. The Project Summary is not the same as a journal article abstract (chapter 7) or a conference abstract (chapter 8), even though the Project Summary is sometimes called an abstract. The Project Summary summarizes work that has yet to be done and is written for a scientific audience.
Globals, Locals, and Mobals
Authors: De Blij Harm
Published: November 2020

Earth may be a planet of shrinking functional distances, but it remains a world of staggering situational differences. From the uneven distribution of natural resources to the unequal availability of opportunity, place remains a powerful arbitrator. Many hundreds of millions of farmers in river basins of Asia and Africa live their lives much as their distant ancestors did, still remote from the forces of globalization, children as well as adults still at high personal risk and great material disadvantage. Tens of millions of habitants of isolated mountain valleys from the Andes to the Balkans and from the Caucasus to Kashmir are as bound to their isolated abodes as their forebears were. Of the seven billion current passengers on Cruiseship Earth, the overwhelming majority (the myth of mass migration notwithstanding) will die very near the cabin in which they were born. In their lifetimes, this vast majority will have worn the garb, spoken the language, professed the faith, shared the health conditions, absorbed the education, acquired the attitudes, and inherited the legacy that constitutes the power of place: the accumulated geography whose formative imprint still dominates the planet. The regional impress of poverty continues to trap countless millions who are and will be born into it and who, globalization notwithstanding, cannot escape it. The “wealth gap” between the fortunate and the less fortunate, still largely a matter of chance and destiny, evinces a widening range resulting from the perpetuation of privilege and power in the so-called global “core” and its international tentacles. Those disparities, represented at all levels of scale, will entail increasing risk in a world of rising anger and weapons of growing destructive efficiency. At the same time, the notion that the world, if not “flat,” is flattening under the impress of globalization is gaining traction. As noted in the preface, the idea that diversities of place continue to play a key role in shaping humanity’s variegated mosaic tends to be dismissed by globalizers who see an increasingly homogenized and borderless world. “Flatness” is becoming an assumption, not merely a prospect, as implied by the titles of numerous books and articles of recent vintage (Fung et al., 2008).
Same Place, Divergent Destinies
Authors: De Blij Harm
Published: November 2020

Dramatic media pictures of desperate would-be mobals clinging to overcrowded boats, climbing over border fences, or running across unguarded wasteland confirm statistical data: males are in the vanguard of unregulated as well as legal transnational migration. Less graphic photography of the average business-class section of a 747 flying from Los Angeles to Hong Kong would reveal that most of the comfortable globals en route are male as well. But scrutinize a daytime picture of an African or Asian village, and you are likely to notice that among the locals, women outnumber men, whether working in the fields, carrying water or firewood, preparing food, or tending children. If the Earth seems flat, this is far more so for males than for females. Even in the same village, in the same house, the destinies of boys and girls diverge startlingly, and not only in rural villages in the global periphery. Equality of the sexes in employment, income, political influence, and other circumstances is an elusive goal even in the richest countries of the global core. Northern European countries are often cited as having progressed furthest in this respect, but even there, the playing field (for example, in religious hierarchies) is not completely level. Nor does growing wealth guarantee progress in closing the gender gap. Male dominance is a deeply embedded tradition that has a way of trumping fairness: in modern Japan, where women have made significant strides by many measures, the Minister of Health and Welfare in July 2007 publicly referred to the role of women as being “birth-giving machines” (Economist, 2007d). When China in the late 1970s embarked on its economic reforms, one key to success was deemed to lie in bringing its population spiral under control. China’s “one child only” policy had the desired result, but in effect it frequently meant one male child only as tens of millions of pregnancies were aborted to ensure a male heir. Millions more female infants were and are abandoned, giving rise to an international adoption industry that is almost exclusively female. Today, economically booming China has a demographic surplus of some 20 million males, with troubling implications for the future.
Atomic Structure and Isotopes
Authors: Oriakhi Christopher O.
Published: November 2020

John Dalton proposed his theory of the atom in 1808 based on experimental data and chemical laws known in his day. The theory states that: 1. All chemical elements are made up of tiny indivisible particles called atoms. 2. Atoms cannot be created or destroyed. Chemical reactions only rearrange the manner in which atoms are combined. 3. Atoms of the same element are identical in all respects and have the same masses and physical and chemical properties. Atoms of different elements have different masses as well as different physical and chemical properties. 4. Combination of elements to form a compound occurs between small, whole-number ratios of atoms. Dalton’s theory resulted in the formulation of the law of conservation of mass and the law of multiple proportions. In a chemical reaction matter is neither created nor destroyed. The mass of products is equal to the mass of the reactants. If two elements form more than one compound between them, the masses of one element that combine with a fixed mass of the second element are in a ratio of whole numbers. Nitrogen and oxygen combine to form different compounds such as NO, NO2, and N2O. According to this law the number of nitrogen to oxygen atoms in these compounds should be a simple ratio of two small whole numbers. This is one of the basic laws of stoichiometry, as we shall see in chapter 9. An atom consists of a central nucleus, which contains roughly 99.9% of the total mass of the atom, and a surrounding cloud of electrons. The nucleus is composed of two kinds of particles, the protons and the neutrons, which are collectively known as the nucleons. The proton is positively charged while the neutron is electrically neutral. The electrons have a negative charge and surround the nucleus in “shells” of definite energy levels. (Note: energy level will be discussed in chapter 10.) In a neutral (unreacted) atom, the number of electrons is equal to the number of protons, so the atom has a charge of zero.
Introduction
Authors: Fish Stanley
Published: November 2020

Not long ago, there was a time when I was responsible for a college with close to 30 departments and units, a budget of between 50 and 55 million dollars, 400 tenure-track faculty members, 700 staff, 10,000 undergraduate students, 2,000 graduate students, and 17 buildings. On any given day, I had to deal with disciplinary proceedings, tenure and promotion cases, faculty searches, chair searches, enrollment problems, fundraising, community outreach, alumni relations, public relations, curriculum reform, counteroffers, technology failures, space allocation, information systems, chair meetings, advisory committee meetings, deans council meetings, meetings with the provost, student complaints, faculty complaints, parent complaints, and taxpayer complaints. Office hours were 8:30 a.m. to whenever and often extended into the evenings and weekends. Vacations were few and far between. The pressure never relaxed. When I left the job after slightly more than five years, I felt that I had all the time (well, not quite all ) in the world at my disposal, and for a while, spent it by trying to improve everyone I met, whether or not those I ministered to welcomed my efforts. I took my opportunities wherever I found them. While I still lived in Chicago, but after I stepped down as dean, the building next door to mine was bought by a developer. For a long time, no development occurred, and the lawn and bushes were allowed to grow wild. The developer, however, had made the mistake of putting his telephone number on an overlarge sign, and as a reward he received a series of dyspeptic phone calls from me accusing him of being a bad neighbor, an irresponsible landlord, and an all-around no-goodnik. During the same period, I would go into a store or stand in a ticket line and was often greeted by someone who asked, “And how are you today, young man?” That is my least favorite salutation, and I quickly delivered a lecture and, I trust, a bit of improvement: “When you call someone who is obviously not young ‘young man,’ what you are doing is calling attention to his age and making him feel even older than he is; don’t do it again!” I delivered an even longer lecture to the blameless fastfood workers who routinely handed me a bagel along with a small container of cream cheese and a plastic knife that couldn’t cut butter.
Generalized Anxiety Disorder
Authors: Starcevic, MD, PhD Vladan
Published: November 2020

The main characteristics of generalized anxiety disorder (GAD) are chronic pathological worry, other manifestations of nonphobic anxiety, and various symptoms of tension. Physical symptoms of anxiety are usually less prominent in GAD than in panic disorder, but they can still be an important component of clinical presentation. Behaviors that are often seen in other anxiety disorders, such as overt avoidance, are conspicuously absent. Unlike all other anxiety disorders, it is more likely for GAD in clinical setting to co-occur with a primary condition for which help has been sought–usually depression or other anxiety disorder–than to be the main reason for seeking professional help. Generalized anxiety disorder is one of the more controversial members of the family of anxiety disorders: it seems that almost every aspect of GAD has provoked debates that do not show signs of abating. Paradox, disagreement, debate, and controversy are the words most commonly associated with GAD. It is small wonder then that the list of ‘‘hot topics’’ related to GAD could be very long indeed. Listed below is a selection of issues thought to represent adequately a more comprehensive list…. 1. What are the characteristic features of GAD that would help in its conceptualization? Pathological worry, other cognitive aspects of anxiety, manifestations of tension, and/or (some) symptoms of autonomic arousal? What combination of these features would ensure that GAD is diagnosed adequately and recognized in clinical practice? 2. What is the relationship between pathological worry and GAD? 3. How can different views on what constitutes the essence of GAD be reconciled? Is GAD a single entity or are there two or more ‘‘types’’ of GAD with distinct clinical characteristics? 4. How is GAD related to depressive disorders, other anxiety disorders, and personality disturbance? Where are its boundaries? In view of its close relationship with depression, should GAD be classified along with depression and perhaps renamed accordingly? 5. Can GAD exist on its own, without depression or other anxiety disorders? What could be features specific enough for GAD that would allow it to establish itself as an independent and valid psychopathological and diagnostic entity? 6. What are the pathophysiological correlates of pathological worry and other aspects of chronic anxiety in GAD? 7. What are the underlying mechanisms and purpose of pathological worry in GAD? What is the meaning of chronic anxiety?
What is Psychosis?
Authors: Compton Michael T , Broussard Beth
Published: November 2020

We began the Preface with a list of questions that people experiencing psychosis and their family members often have. As we mentioned, an episode of psychosis can be frightening, confusing, and painful for the individual going through it and for his or her family members. We also noted that this book is meant to help readers through a very difficult time by providing much needed information. Part 1 of this book, Answering Your Basic Questions, focuses on explaining some of the most important facts about psychosis. This chapter addresses the first basic question, what is psychosis? In this chapter, we define what psychosis is and then dispel some myths by describing what psychosis is not. We then briefly describe what percentage of people develop psychosis and when it usually first begins. Next, we present the idea of a “psychosis continuum,” which means that experiences of psychosis can differ in level of seriousness. We then set the stage for later chapters by briefly introducing schizophrenia (one of the illnesses that is related to psychosis) and several other topics to come later in the book, including causes of psychosis, treatments, and recovery. Psychosis is a form of mental illness. A mental illness affects a person’s thoughts, feelings, and behaviors. Like physical illnesses, mental illnesses are treatable. Psychosis is a treatable mental illness syndrome. You may be familiar with some other mental illness syndromes, such as depression, posttraumatic stress disorder, and panic attacks. So what exactly does psychosis mean? Psychosis is a word used to describe a person’s mental state when he or she is out of touch with reality. For example, a person might hear voices that are not really there (auditory hallucinations) or believe things that are not really true (delusions). Psychosis is a medical condition that occurs due to a dysfunction in the brain. People with psychosis have difficulty separating false personal experiences from reality. They may behave in a bizarre or risky manner without realizing that they are doing anything unusual. Similar to any other health condition, psychosis consists of a combination of both symptoms that patients experience and signs that doctors observe.