bluuebunny/crossref_metadata_2025 huggingface dataset:
Rivers
Authors: Dunne Thomas , Kerry Mertes Leal Anne
Published: November 2020

River basins and river characteristics are controlled in part by their tectonic setting, in part by climate, and increasingly by human activity. River basins are defined by the tectonic and topographic features of a continent, which determine the general pattern of water drainage. If a major river drains to the ocean, its mouth is usually fixed by some enduring geologic structure, such as a graben, a downwarp, or a suture between two crustal blocks. The largest river basins constitute drainage areas of extensive low-lying portions of Earth’s crust, often involving tectonic downwarps. The magnitude of river flow is determined by the balance between precipitation and evaporation, summed over the drainage area. Seasonality of flow and water storage within any basin are determined by the seasonality of precipitation in excess of evaporation, modified in some regions by water stored in snow packs and released by melting, and by water stored in wetlands, lakes, and reservoirs. Increasingly the flows of rivers are influenced by human land use and engineering works, including dams, but in South America these anthropogenic influences are generally less intense and widespread than in North America, Europe, and much of Asia. Thus the major rivers of South America can be viewed in the context of global and regional tectonics and climatology. For reference, figure 5.1 outlines South America’s three largest river basins—the Orinoco, Amazon, and Paraguay-Paraná systems—while figure 5.2 shows the locations of rivers referred to in the text against a background of the continent’s density of population per square kilometer. The geologic history of South America has bequeathed to the continent a number of structural elements that are relevant to the form and behavior of its three major river systems. These structural elements are (1) the Andes; (2) a series of foreland basins, approximately 500 km wide immediately east of the Andes and extending southward from the mouth of the Orinoco to the Chaco-Paraná basin, where the crust is depressed by the weight of the Andes and the sediment derived from the mountains; (3) the Guiana and Brazilian shields reflecting Precambrian cratons and orogenic belts of mostly crystalline metamorphic rocks, partly covered with flat-lying sedimentary rocks and deeply weathered regolith; and (4) the Central Amazon Basin, a large cratonic downwarp with some graben structures dating back to early Paleozoic time, which runs generally east-west between the two shields, connecting the foreland basins to the west with a graben that localizes the Amazon estuary at the Atlantic coast.
Tropical Forests of the Lowlands
Authors: Furley Peter A.
Published: November 2020

Most of South America lies within the tropics, and lowland tropical ecosystems make up the majority of its landscapes. Although there is great concern for the Amazon ecosystem, the largest of the world’s tropical forests, there are many other fascinating and in some cases more endangered types of lowland forest. Such forests may be defined as lying below 1,000 m above sea level, although it is difficult to set arbitrary limits (Hartshorn, 2001). The two main lowland moist evergreen forests are the Hylea (a term coined by Alexander von Humboldt to denote rain forests of the Amazon Basin) and the much smaller Chocó forest on the Pacific coast between Panama and Ecuador. Two related yet distinctive types of forest are the Mata Atlântica or Atlantic moist evergreen forest and the Mata Decidua or dry deciduous forest, including the caatinga woodland, which is both deciduous and xerophytic (Rizzini et al., 1988). The latter two formations are among the most threatened of all South American forests. Lowland forests vary from dense and multilayered to open and single-layered, from evergreen to deciduous, and from flooded or semi-aquatic to near-arid. Tree heights range from 30 to 40 m with emergent trees reaching over 50 m, to forests where the tallest trees barely attain 20 m (Harcourt and Sayer, 1996; Solorzano, 2001). However, because of its extent and importance, Amazonia will form the principal focus of this chapter. Amazonia covers a vast area (>6 × 106 km2) and contains some 60% of the world’s remaining tropical forest. The Amazon and Orinoco basins influence not only regional climates and air masses, but also atmospheric circulation patterns both north and south of the Equator. The sheer size and diversity of Amazonia exhausts a normal repertoire of grandiose adjectives. The Amazon may or may not be the longest river in the world but it is by far the greatest in terms of discharge, sending around one fifth of the world’s fresh water carried by rivers to the oceans(see
chapter 5; Eden, 1990; Sioli, 1984). The drainage basin is twice as large as any other of the world’s catchments.
Eye Rotations, the Extraocular Muscles, and Strabismus Terminology
Authors: Wong Agnes
Published: November 2020

To understand how eye muscles move the eyeball, it is necessary to understand the geometry of the eye and the functions of the muscles. The eyeball rotates about three axes: horizontal, vertical, and torsional. These axes intersect at the center of the eyeball. Eye rotations are achieved by coordinated contraction and relaxation of six extraocular muscles—four rectus and two oblique—attached to each eye. The action of the muscles on the globe is determined by the point of rotation of the globe, as well as the origin and insertion of each muscle. Recent evidence suggests that the muscles also exert their effects on the globe via the extraocular muscle pulleys. Considering that we make at least 100,000 saccades alone each day, it is not surprising that many extraocular muscles are very resistant to fatigue. Extraocular muscles are also different from other skeletal muscles in many respects. For example, eye muscle fibers are richly innervated, and each motoneuron innervates only 10–20 muscle fibers, the smallest motor unit known in the body. Extraocular muscles also have more mitochondria and a higher metabolic rate than other skeletal muscles. Thus, extraocular muscles are one of the fastest contracting muscles. This property allows animals to shift gaze swiftly, so that they can avoid approaching predators or detect prey in the vicinity. The unique immunologic and physiologic properties of extraocular muscles may also explain why they are more susceptible to certain disease processes, such as Grave’s disease and chronic progressive external ophthalmoplegia, but more resistant to others such as Duchenne’s dystrophy, which mainly affects skeletal muscles in the rest of the body. The eyeball rotates about three axes: x-axis (naso-occipital or roll axis), y-axis (earthhorizontal or pitch axis), and z-axis (earth-vertical or yaw axis). Ductions refer to monocular movements of each eye. They include abduction, adduction, elevation (sursumduction), depression (deorsumduction), incycloduction or incyclotorsion, and excycloduction or excyclotorsion (see table on opposite page). Versions refer to binocular conjugate movements of both eyes, such that the visual axes of the eyes move in the same direction. They include dextroversion, levoversion, elevation (sursumversion), depression (deorsumversion), dextrocycloversion, and levocycloversion (see table).
Nystagmus
Authors: Wong Agnes
Published: November 2020

Nystagmus is involuntary eye oscillations initiated by slow eye movements that drive the eye away from the target. In contrast, saccadic dyskinesia consists of involuntary, fast eye movements that take the fovea off target. Nystagmus usually arises from lesions in the 1. Vestibulo-ocular system (VOR) 2. Gaze-holding system 3. Smooth pursuit and optokinetic system. 1. Pendular versus jerk ■ Pendular (see A in the figure below): both phases are slow eye movements. ■ Jerk (see B, C, and D in the figure below): one phase consists of fast eye movements (quick phase), and the other consists of slow eye movements. By convention, the direction of nystagmus is named after the direction of quick phases that return the eye to the target. 2. Plane: horizontal, vertical, torsional, or combined form (e.g., rotary, elliptical) 3. Conjugacy ■ Conjugate: Both eyes move in the same direction with similar amplitude and frequency. ■ Disconjugate: Both eyes move in the same direction with different amplitude and frequency (e.g., internuclear ophthalmoplegia). ■ Disjunctive: The eyes move in opposite directions (e.g., oculomasticatory myorhythmia seen in Whipple’s disease).
ReAction!
Authors: Griep Mark A. , Mikasen Marjorie L.
Published: November 2020

ReAction! gives a scientist's and artist's response to the dark and bright sides of chemistry found in 140 films, most of them contemporary Hollywood feature films but also a few documentaries, shorts, silents, and international films. Even though there are some examples of screen chemistry between the actors and of behind-the-scenes special effects, this book is really about the chemistry when it is part of the narrative. It is about the dualities of Dr. Jekyll vs. inventor chemists, the invisible man vs. forensic chemists, chemical weapons vs. classroom chemistry, chemical companies that knowingly pollute the environment vs. altruistic research chemists trying to make the world a better place to live, and, finally, about people who choose to experiment with mind-altering drugs vs. the drug discovery process. Little did Jekyll know when he brought the Hyde formula to his lips that his personality split would provide the central metaphor that would come to describe chemistry in the movies. This book explores the two movie faces of this supposedly neutral science. Watching films with chemical eyes, Dr. Jekyll is recast as a chemist engaged in psychopharmaceutical research but who becomes addicted to his own formula. He is balanced by the often wacky inventor chemists who make their discoveries by trial-and-error.
Evaluation and Spectrum of Orbital Diseases
Authors: Douglas Raymond S. , Goldberg Robert A.
Published: November 2020

Although orbital disorders are not frequently encountered in the comprehensive ophthalmologist’s practice, it is essential to be able to diagnose patients with orbital disease and manage them accordingly. Various disease processes can affect the orbit. This chapter endeavors to provide a thoughtful, stepwise, and logical approach to the evaluation of orbital disease. The discussion begins with differential diagnosis, adds an intelligent history-taking and physical examination, and then focuses on efficient use of diagnostic tests to finally arrive at the correct diagnosis. The staging and management of two common orbital disorders, orbital inflammation and thyroid-associated ophthalmopathy, will also be discussed. The differential diagnosis of orbital disease is extensive, and most listings of orbital disease divide the causes between histopathologic and mechanistic categories. This type of grouping is intellectually sound and scientifically useful but does not provide a framework that the clinical practitioner can easily grasp and directly use in sorting through the differential diagnosis of any given patient. In broad terms, orbital disease can be considered in terms of location, extent, and biologic activity. The classification used in this chapter is broken down along clinical lines and takes advantage of the fact that the orbit has a somewhat limited repertoire of ways that it can respond to pathologic conditions. Orbital disease can be categorized into five basic clinical patterns: inflammatory, mass effect, structural, vascular, and functional. Although many cases cross over into several categories, the vast majority of clinical presentations fit predominantly into one of these patterns. As the clinician walks through each step of the evaluation process—history, physical examination, laboratory testing, orbital imaging—a conscious effort should be made to categorize the presentation within this framework. If the practitioner approaches orbital disease with this framework of discrete patterns of clinical presentation, then at every step of the diagnostic pathway (history, physical examination, orbital imaging studies, and special tests), he or she can draw from a defined set of differential diagnoses that characterize each pattern of orbital disease and use that information to efficiently and confidently orchestrate diagnosis and management.
School-to-Jobs Implementation Manual: Including Fidelity and Outcome Measures
Authors: Oyserman Daphna
Published: November 2020

Greet participants as they enter and take attendance in a notebook—noting if on time, late, or absent. This ensures that you will quickly learn all participants’ names. Knowing names allows you to refer to participants by name, which is very positively reinforcing and increases engagement.
If you need help learning names, photograph participants in Session 1; make photo nametags with names large enough for you to read and have participants pick them up at the beginning of each session (and leave them behind). Repeat names each time a person participates. This enormously increases engagement. Pay attention to the flow so that time will be adequate. Stick to the session theme by eliciting discussion focused on theme and weaving focus back to theme. This is not counseling or therapy. Do not delve deeply into a student’s life, problems, or issues. Do not go off on tangents about other information. This is not career counseling or academic guidance. Positively reinforce both speakers and listeners. Positive reinforcement is task oriented. It is specific and helps participants behave in ways that will help them stay in school. Positive reinforcement is not simply saying “good” or “great job!” or “interesting comment.” Positive reinforcement is specific; this means saying what was good or interesting about the job or comment. Examples would be (Session 1) “That was a good introduction; you gave a skill John has to succeed in next year in school.” Or (Session 10) “Great! Your group came up with questions instead of jumping right in with a solution.” Use the outline agenda as a structure guide for participants. Hang the agenda prior to the start of each session. Bring newsprint and writing material to each training session. Write participant responses on newsprint so their work in the session is visible. The newsprint serves to structure the flow and highlight themes. Responses that focus on themes relevant to the session should be organized physically on the page by placing content about a theme together without labeling and later labeling each theme as part of the connecting discussion.
Down Syndrome
Authors: Hooper Stephen R. , Hammer Julie
Published: November 2020

Down syndrome (DS) is the most common genetic cause of significant intellectual disability in humans. It was one of the first chromosomal disorders of humans to be associated with intellectual disabilities and, as such, has provided an evidence-based foundation from which work on many different disorders has been launched. John Langdon Down first described this syndrome in 1866 using the term mongoloid idiocy. The initial clinical description of DS comprised physical features (e.g., epicanthal folds, flat and broad face, enlarged tongue, microcephaly, short stature) and cognitive characteristics (e.g., intellectual impairment, fine and gross motor coordination problems, poor speech articulation). He also described a relatively positive personality in these individuals. Contemporary topographical descriptions are remarkably similar to Down’s description nearly 150 years ago, but a variety of other healthrelated issues have been uncovered since that time including congenital cardiac abnormalities, hypotonia, hearing and visual impairments, hypothyroidism, and precocious aging (Rasmussen, Whitehead, Collier, and Frias 2008). In accordance with the core tenets of this text, in this chapter we discuss epidemiology, etiology, and what is known about core pathophysiological mechanisms in DS; neurological abnormalities, including contemporary findings in neuroimaging; neurocognitive and socialbehavioral manifestations; and emergent evidencebased treatment efforts. The chapter concludes with a brief discussion of the phenotype-genotype linkages for DS, and a review of the priorities set by a national panel of experts in DS (Rasmussen et al. 2008). When compared to other congenital abnormalities, DS represents one of the most common disorders. Contemporary prevalence estimates indicate the occurrence of DS in approximately 9.0–11.8 (Shin et al. 2009) to 13.66 (Canfield et al. 2006) per 10,000 live births. The rate of infants born with DS also has a strong relationship with increasing maternal age. For example, a 20-year-old mother has a 1 in 1,923 chance of giving birth to an infant with Down syndrome, whereas the chance for a 49-year-old mother is 1 in 12 (Prescott 1988). The cause of this phenomenon, however, is not well understood (Lamb and Hassold 2004).
Neurocognitive Outcomes in Childhood Cancer: Effects of Disease and Treatment on Brain Development and Learning
Authors: Armstrong F. Daniel , Goldman Maria L.
Published: November 2020

Childhood cancer is a rare disease, accounting for only 1% of all malignancies in humans of all ages. In 2007, approximately 10,400 new cases of cancer were diagnosed in children 14 years of age and younger (American Cancer Society 2007). Significant advances in diagnostic techniques and tailored treatments during the past three decades have increased the 5-year survival rate for all cancers to over 80% (Twombly 2007). For acute lymphoblastic leukemia (ALL), the most common form of childhood cancer, the current survival rate is approaching 90% (Pui and Howard 2008). Better survival has led to increased awareness and focus on the consequences of cancer treatment, called late effects. The Children’s Oncology Group has developed and published guidelines for monitoring childhood cancer survivors for late effects in nearly every organ system (Landier et al. 2004), with a recent growing interest in those affecting cognitive, academic, social, and behavioral function (Nathan et al. 2007), which are the focus of this chapter. It was long assumed that a cancer diagnosis and the severe toxicity associated with treatment was such a traumatic event that significant adverse psychological consequences were inevitable. Recent, large reports from the Childhood Cancer Survivorship Study and reviews of smaller studies suggest that this is not the case for the majority of children and adolescents treated for and surviving cancer (Eiser, Hill, and Vance 2000; Zebrack et al. 2002; Zeltzer et al. 2009). With the exception of children who experience central nervous system (CNS) cancer or cancer treatment (Zebrack et al. 2004), most childhood cancer survivors are not significantly different from the general population on measures of depression (Phipps and Srivastava 1999), selfesteem (Noll et al. 1999), hopefulness (Ritchie 2001), or posttraumatic stress disorder (PTSD). Some children experience symptoms of posttraumatic stress during acute treatment, but these symptoms diminish over time (Phipps et al. 2006). For children with CNS cancer or who receive treatment that affects the CNS, the picture is somewhat different, with poorer emotional and social functioning, neurocognitive function, and overall health-related quality of life (HRQL) reported in this subpopulation (Calaminus et al. 2000; Vannatta et al. 2007).
Cognitive and Behavioral Challenges of Chronic Kidney Disease
Authors: Icard Phil , Hooper Stephen R.
Published: November 2020

Chronic kidney disease (CKD) affects children and adults of all ages. The term encompasses patients with kidney function below approximately 75% of normal and extends down to include those with dialysis or kidney transplant–dependent kidney failure. With progressively less kidney function, the body begins to accumulate waste products that the kidney fails to clear and is at risk for an ever-increasing number and variety of complications related to kidney failure. Over the past two decades, the neurodevelopmental effects of CKD have been studied in numerous modestly sized studies (Gipson et al. 2004). Further, progress in the medical management of children with CKD over the past decades has resulted in increased patient survival (USRDS 2003). Despite these important advances in the care of children with CKD, recent investigations have continued to reflect a variety of cognitive and social-behavioral concerns associated with CKD. This chapter provides an overview of the work conducted to date addressing the cognitive and behavioral functioning of children and adolescents with CKD. This overview will include an initial discussion of neurological findings, including structure imaging and electrophysiological studies. Additionally, the neurocognitive and social-behavioral findings in CKD are described. Finally, we provide data addressing the developmental continuity of these types of challenges in adult survivors of childhood-onset CKD. The relationship between CKD and central nervous system (CNS) dysfunction has a longstanding history in the literature (Gipson et al. 2004). Early studies showing high rates of developmental delay and encephalopathy in pediatric CKD patients called attention to the significant neurological impairments caused by kidney disease (Polinsky, Kaiser, and Stover 1987). Chronic kidney disease impacts the nervous system in many ways, perhaps most significantly by not effectively filtering neurotoxic chemicals and metabolites from the bloodstream. Over time, the circulation of harmful biochemicals through the brain and its periphery has the potential to significantly impact the structure and organization of the nervous system. Even early treatments for CKD (e.g., aluminum phosphate binders) were found to have an averse affect on the developing brain, and have subsequently been eliminated from contemporary treatment protocols.
Intrauterine and Postnatal Exposure to Tobacco and Secondhand Smoke and Child Cognitive and Behavioral Development
Authors: Poole-Di Salvo Elizabeth
Published: November 2020

Children’s involuntary exposure to tobacco smoke is a common and substantial health problem that has been receiving increasing attention from the pediatric, public health and research communities. According to the 2006 Surgeon General’s Report, there is no safe level of tobacco smoke exposure, yet at least 30% of children in the United States live in households with at least one adult smoker, and nearly 60% have evidence of recent exposure (Machlin, Hill, and Liang 2006). Tobacco smoke exposure has been causally linked to numerous adverse health outcomes and is currently a leading preventable cause of both low birth weight and sudden infant death syndrome, and a major contributor to lower respiratory infections, otitis media, and increased asthma severity (American Academy of Pediatrics, Committee on Environmental Health 1997; Cook and Strachan 1999; DiFranza et al. 2004). Recently, associations between tobacco smoke exposure and other childhood health problems, such as increased rates of dental caries (Aligne et al. 2003; Iida et al. 2007), food insecurity (Cutler et al. in press), and the metabolic syndrome (Weitzman et al. 2005) have been identified. As discussed in this chapter, a growing human and animal literature, which expands upon a more than 25-year-old body of work, also indicates that involuntary exposure to tobacco smoke during the pre- and/or postnatal periods is associated with adverse cognitive and behavioral outcomes in children. Tobacco smoke exposure has been associated with decrements in IQ, problems with learning and memory, difficulty with auditory processing, neonatal hyperactivity, attention-deficit hyperactivity disorder (ADHD), internalizing and externalizing behavioral problems, and conduct disorder. Animal models have provided evidence that tobacco is toxic to the developing brain, and there are plausible biologic pathways that appear to mediate these effects. Exciting new studies have begun to identify specific genes that play a role in the relationship between tobacco smoke exposure and adverse cognitive and behavioral outcomes in children. The term “secondhand smoke” (SHS), also referred to as “environmental tobacco smoke” (ETS), refers to the smoke that is exhaled from a smoker’s lungs, as well as the smoke from the smoldering end of a cigarette.
Pediatric Carbon Monoxide Poisoning
Authors: Hopkins Ramona O.
Published: November 2020

Carbon monoxide (CO) exposure has been described ever since humans developed products of combustion (e.g. fire, burning charcoal). The Romans realized that CO poisoning leads to death (Penney 2000). Coal fumes were used in ancient times for execution, and the deaths of two Byzantine emperors are attributed to CO poisoning (Lascaratos and Marketos 1998). Admiral Richard E. Byrd developed CO poisoning during the winter he spent alone in a weather station deep in the Antarctic interior (Byrd 1938). Further, CO poisoning took the life of tennis player Vitas Gerulaitis (“Died, Vitas Gerulaitis,” 1994; Lascaratos and Marketos 1998) and may have contributed to Princess Diana’s accidental death in 1997 (Sancton and Macleod 1998). Carbon monoxide is a colorless, tasteless, odorless gas by-product of the combustion of carbon-containing compounds such as natural gas, gasoline, kerosene, propane, and charcoal. The most common sources of CO poisoning are internal combustion engines and faulty gas appliances (Weaver 1999). Carbon monoxide poisoning can also occur from space heaters, methylene chloride in paint removers, and fire (Weaver 1999). The most frequent causes of pediatric CO poisoning are vehicle exhaust, dysfunctional gas appliances and heaters, and charcoal briquettes (Kind 2005; Mendoza and Hampson 2006). Less common sources of CO poisoning include riding in the back of pickup trucks, and while swimming and recreational boating (Hampson and Norkool 1992; Silvers and Hampson 1995). Among pediatric populations, minorities are disproportionately affected by CO poisoning compared to Caucasians, and Latinos and non-Latino blacks were more commonly poisoned by charcoal briquettes used for cooking or heating (Mendoza and Hampson 2006). Carbon monoxide is the leading cause of poisoning injury and death worldwide (Raub et al. 2000) and accidental and intentional poisoning in the United States. In the United States carbon monoxide poisoning results in approximately 40,000 emergency department visits (Hampson 1999) and 800 deaths per year (Piantadosi 2002). Children are particularly venerable to CO poisoning. The Center for Disease Control reports children younger than 4 years have the highest incidence of unintentional CO poisoning but the lowest death rates (2005).
Writing the Outcomes and Impacts Section
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

All good proposals must come to an end. In this chapter, we examine conventional ways in which authors summarize and conclude their Project Descriptions. We consider project timelines, lists of expected outcomes, and statements of broader impacts. By the end of this chapter, you should be able to ■ Develop a project timeline ■ Generate a list of expected outcomes ■ Suggest broader impacts of your proposed work ■ Reinforce the importance of your proposed work in concluding remarks As you work through the chapter, you will write the closing section of your own Project Description. The Writing on Your Own tasks throughout the chapter guide you step by step as you do the following: 14A Create a project timeline 14B Create a list of expected outcomes 14C Conclude the proposed work
14D Complete the Outcomes and Impacts section Like the previous sections of the Project Description (chapters 12 and 13), there is no one right way to end a proposal. However, proposal guidelines often instruct authors to include a projected timeline, a list of expected outcomes, a summary of objectives, and/or a statement of relevance or broader impacts in their concluding remarks. For example, the ACS Division of Analytical Chemistry Graduate Fellowship announcement (excerpt 11A) asks for a statement that links “the relevance of [the proposed] work to analytical chemistry.” The NSF Grant Proposal Guide (see excerpt 15B) asks for “objectives for the period of the proposed work,” their “expected significance,” and their “relationship to longer-term goals of the PI’s project.” Moreover, the PI must describe “as an integral part of the narrative, the broader impacts of the proposed activities.” Not surprisingly, each of the authors of our 22 CAREER proposals approached this task slightly differently. We examine several of their approaches in this chapter. We begin with an excerpt that you can read and analyze on your own (excerpt 14A), specifically, the conclusion to Harpp’s proposal regarding plume-ridge interaction in the Galápagos. She includes a formal timeline (titled “Project Schedule”) and conclusions for her work.
Formulas of Compounds and Percent Composition
Authors: Oriakhi Christopher O.
Published: November 2020

Percent means “parts per 100” or “part divided by whole, multiplied by 100.” If the formula of a compound is known, one can easily calculate the mass percent of each element in the compound. By definition, the percent composition of a compound is the mass percent of each element in the compound. The molar mass represents 100% of the compound. % Element = Mass of element/Formula mass ×100 The following steps are helpful in calculating the percent composition if the formula of the compound is known. 1. Calculate the formula mass or molar mass of the compound 2. Calculate the percent composition by dividing the total mass of each element in the formula unit by the molar mass and multiplying by 100. Aspirin, which is commonly used as a pain reliever, has the chemical composition C9H8O4. Calculate the percent composition of aspirin.
What Causes Primary Psychotic Disorders Like Schizophrenia?
Authors: Compton Michael T , Broussard Beth
Published: November 2020

Doctors and researchers have been able to identify the causes of a variety of medical conditions, such as the common cold, a heart attack, and gout, to name a few. For example, there are different types of viruses that cause the symptoms of a common cold. By knowing what causes a medical problem, doctors are able to treat the condition in the most focused way possible. In the previous chapter, three general categories of causes of psychosis were presented: medical causes, substances, including certain drugs of abuse and several medicines, and a number of psychiatric illnesses. This chapter presents what is currently known about the causes of the third of these, psychiatric illnesses, especially primary psychotic disorders like schizophrenia. Some health conditions have a single, straight-forward cause. As mentioned earlier, a common cold is caused by a virus. However, many illnesses do not have a single identifiable cause. Rather, they are caused by a combination of risk factors. A risk factor is any event, exposure, or entity that occurs before the illness and that research has shown plays a role in causing the illness. For example, cigarette smoking is a well-known risk factor for lung cancer. Smoking occurs before the lung cancer develops, and researchers have proven that smoking cigarettes plays a part in causing many cases of lung cancer. Because schizophrenia and related psychotic disorders are such complex illnesses, it is sometimes unclear if some of the risk factors truly occur before the illness. Some risk factors may make some people more psychosis-prone. In other words, some risk factors are best thought of as increasing one’s tendency towards psychosis rather than actually causing psychosis. Over the past several decades, researchers have identified some of the likely causes of complex medical conditions like diabetes, high blood pressure, and psychosis. For each of these, as is true of most medical conditions, there is no single cause. Rather, a number of risk factors, both internal (like certain genes) and external (like exposures that stress the body, such as stressful life events or drugs) combine in complex ways to bring about the illness.
Handbook of AIDS Psychiatry
Authors: Cohen Mary Ann , Goforth Harold , Lux Joseph , Batista Sharon , Khalife Sami , Cozza Kelly , Soffer Jocelyn
Published: November 2020

The Handbook of AIDS Psychiatry is a practical guide for AIDS psychiatrists and other mental health professionals as well as for other clinicians who work with persons with HIV and AIDS and a companion book to the Comprehensive Textbook of AIDS Psychiatry (Cohen and Gorman, 2008). The Handbook provides insights into the dynamics of adherence to risk reduction and medical care in persons with HIV and AIDS as well as strategies to improve adherence using a biopsychosocial approach. Psychiatric disorders can accelerate the spread of the virus by creating barriers to risk reduction. Risky sexual behaviors and sharing of needles in intravenous drug users account for the majority of new cases each year. Delirium, dementia, depression, substance dependence, PTSD, and other psychiatric disorders complicate the course and add considerably to the pain and suffering of persons with AIDS. HIV infection and AIDS also are risk factors for suicide, and the rate of suicide has been shown to be higher in persons with AIDS. Psychiatric care can help prevent HIV transmission through recognition and treatment of substance-related disorders, dementia, and mood disorders such as mania. Comprehensive, coordinated care by a multidisciplinary AIDS team, including AIDS psychiatrists, can provide a biopsychosocial approach that is supportive to patients, families, and clinicians. Psychiatric interventions are valuable in every phase of infection, from identification of risk behaviors to anticipation about HIV testing; from exposure and initial infection to confirmation with a positive HIV antibody test; from entry into systems of care to managing complex antiretroviral regimen; from healthy seropositive to onset of first AIDS-related illness; from late stage AIDS to end-stage AIDS and death. There is no comprehensive handbook of AIDS psychiatry to guide clinicians in providing much needed care. The Handbook of AIDS Psychiatry is a practical pocket guide that provides protocols for the recognition and treatment of the psychiatric disorders most prevalent in persons with AIDS and most relevant for primary physicians, infectious disease specialists, and other caregivers because of their impact on health, adherence, behavior, and quality of life.
Intraoperative Hyphema
Authors: Moura Filho Edney R. , Sit Arthur J.
Published: November 2020

Hemorrhage is a common complication in trabeculectomy. Hyphema can be a manifestation of an intraoperative hemorrhage and has numerous potential causes. Although generally self-limited, severe complications are possible due to intraoperative hyphemas, and effort should be made to prevent or minimize their occurrence. Large clinical trials suggest that intraoperative hyphema is a common complication of filtration surgery. In the Advanced Glaucoma Intervention Study (AGIS), the investigators found a 13% prevalence of intraoperative anterior chamber bleeding in eyes treated with trabeculectomy (67 of 513 eyes). Similarly, the Collaborative Initial Glaucoma Treatment Study (CIGTS) found a hyphema prevalence of 8% in eyes (37 of 465 eyes) treated surgically. More recently, the Tube Versus Trabeculectomy Study reported an intraoperative hyphema rate of 3% (3 of 105 eyes) in the trabeculectomy arm of the trial. Ocular risk factors for an intraoperative hyphema include elevated intraocular pressure (IOP), a sudden drop in IOP as a result of filtration surgery, and surgical trauma, particularly an iridectomy. Additionally, the fragile rubeotic iris vessels that may be present in neovascular and inflammatory glaucomas may make those eyes especially susceptible to intraoperative (or postoperative) hyphema. Moreover, patients undergoing glaucoma surgery are often older and have multiple risk factors for intraoperative hemorrhage, including systemic hypertension and vasculopathy, as well as chronic oral anticoagulation therapy (ACT) or antiplatelet therapy (APT). Anterior chamber bleeding leading to a hyphema can occur at multiple stages of filtration surgery. Intraoperative bleeding tends to happen most commonly when cutting the iridectomy, due to direct incision of the major arterial circle of the iris or from damage to the adjacent highly vascular ciliary processes. Hemorrhage also may occur while excising the sclerostomy or following the creation of the paracentesis (especially if there is a large drop in IOP with consequent rupture of fragile rubeotic vessels). During dissection of the partial thickness scleral flap, aqueous or episcleral veins may be cut. If hemorrhage from these vessels is not adequately cauterized, blood may eventually flow into the anterior chamber.
Late Hypotony without Leak
Authors: Tanna Angelo P.
Published: November 2020

Late ocular hypotony without a leak is a relatively common complication after trabeculectomy. In most eyes with a mature trabeculectomy, subconjunctival fibrosis is the rate-limiting factor in filtration; therefore, a reduction in resistance to filtration at the level of the scleral flap usually does not result in hypotony. However, in some eyes there is little subconjunctival fibrosis, and loss of resistance at the level of the scleral flap may result in excessive filtration and hypotony. The use of the antifibrotic agents, 5-flurouracil and mitomycin-C, results in reduced subconjunctival fibrosis and is one factor that increases the likelihood of postoperative hypotony due to the development of a very large and diffuse bleb surface area with the resultant possibility of overfiltration. Understanding how to prevent and manage this complication is important for surgeons who perform trabeculectomy. Myopia and young age are major risk factors for the development of hypotony maculopathy (see Chapter 22 for more information on hypotony maculopathy); however, some eyes tolerate very low intraocular pressures without adverse structural consequences. In eyes with late hypotony without a bleb leak and in the absence of hypotony maculopathy, choroidal detachment, optic disc edema, shallow anterior chamber, or corneal decompensation, patients can be closely monitored without intervention to reverse the hypotony. There are 4 basic mechanisms for hypotony: a bleb (or other wound) leak, overfiltration without an overt leak, excessive uveoscleral outflow by way of a cyclodialysis cleft or retinal tear, and aqueous hyposecretion (see Chapter 10 for more information about early hypotony). The presence of a bleb leak must be excluded by Seidel testing. Fluorescein solution (2%) may be easier to use and allow for better sensitivity for the detection of a leak than the use of a fluorescein-impregnated paper strip. If the anterior chamber is flat, the Seidel test may lead to a false negative result. Over time, scleral flap sutures lose tensile strength, and the scleral flap itself may become thin or even melt.
Obstruction of the Tube/Valve
Authors: Chen Philip P.
Published: November 2020

Tube shunt obstruction is a relatively common complication, with reported rates up to 15%. Tube obstructions can be divided into 2 basic types: 1) distal tube obstruction in the anterior chamber, ciliary sulcus, or pars plana; and 2) proximal tube obstruction at the tubeplate junction. Occasionally tube obstruction may lead the surgeon and patient to believe that the tube shunt was never successful at controlling intraocular pressure (IOP) postoperatively. This complication generally has a high impact on the patient’s postoperative course. Preoperative planning and careful surgical technique can avoid many cases of obstruction. Distal tube obstruction is typically a serious postoperative complication, with a sudden elevation in IOP resulting in pain, inflammation, and worsened vision. The distal end of the tube may be obstructed by blood, fibrin, iris, vitreous, lens material, silicone oil, and/ or viscoelastic. Treatment is tailored to the immediate cause. No matter what the cause of obstruction, if tube repositioning becomes necessary, the use of tube extenders, available either commercially or created with readily available 22-gauge angiocatheter sleeves and silicone tubing (used for nasolacrimal duct intubation), facilitate this procedure if the tube is too short to reposition (see Chapter 30). If a blood clot or fibrin is present, observation with use of ocular hypotensive agents and frequent (every 1–2 hours) application of topical prednisolone acetate, 1% may be sufficient. Tissue plasminogen activator (tPA) also may be injected into the anterior chamber to rapidly resolve the clot. The usual dose of tPA is 12.5 μg in 0.1 cc (0.1 mL) and is readily available from most hospital pharmacies. Multiple injections may be required, but concerns about cost have lessened with the advent of a recombinant form of tPA. In one series of 36 patients treated with tPA after tube shunt surgery, severe hyphema, flat anterior chamber, and profound hypotony were seen after 11% (6 of 55) tPA injections. Blood in the tube may be flushed out with balanced saline solution, using a 27-gauge cannula inserted into the eye through a paracentesis wound. If the tube is buried in the iris, pilocarpine may pull the iris out of the tube.
Complications Specifically Related to Canaloplasty Surgery
Authors: Lewis Richard A.
Published: November 2020

Canaloplasty is a surgical approach for patients with open-angle glaucoma. The objective of the procedure is to enhance circumferential outflow of aqueous from Schlemm’s canal to the collector system, improving outflow without creating a filtering bleb. In the procedure, a microcatheter is threaded into the canal using a standard nonpenetrating approach and then passed for 360 degrees. A polypropylene suture is attached to the catheter. The catheter is then retracted 360 degrees during which time viscodilation is performed. The suture remains in the canal, and the ends of the suture are tied together to place constant tension upon the trabecular meshwork (TM). Theoretically, the tension results in opening of the TM, improving outflow and lowering intraocular pressure (IOP). The procedure has increased in popularity and may be a valuable option for patients with open-angle glaucoma who might be at high risk for filtering surgery complications, such as contact lens wearers, patients on blood thinners, and those patients who already failed filtering surgery in the other eye. With the increased popularity of canaloplasty, knowing how to prevent and manage complications of this procedure are crucial skills for today’s glaucoma surgeon. The notion of enhancing circumferential outflow arose from studies of an earlier nonpenetrating procedure, viscocanalostomy (see Chapter 52). In this procedure, a Descemet’s membrane window is created under a scleral flap, and the outflow system is dilated with viscoelastic for 1–2 clock hours. However, in canaloplasty, 360-degree viscodilation is performed, and a tensioning suture is left in Schlemm’s canal to promote canal distension and aqueous outflow. Passing the microcatheter and completing a successful canaloplasty requires specific steps and careful attention to detail. The procedure may be performed under local, regional, or general anesthesia. Fixation of the globe is the first step, using either a corneal or rectus suture. Then, a half-thickness, 4 mm limbus-based scleral flap is created, followed by a deeper scleral flap, which unroofs the canal. The dissection is then taken forward onto Descemet’s membrane to allow for creation of a Descemet’s window, and the deep flap is excised. Schlemm’s canal is next catheterized 360 degrees.
How Brooklyn Became Cool
Authors: Zukin Sharon
Published: November 2020

It’s one o’clock in the morning on a warm October night, and the streets of northern Brooklyn are eerily deserted. The hulks of warehouses and the chimney of the old Domino sugar refinery stand guard along the waterfront, while grim industrial buildings hunker down in the shadow of the Brooklyn-Queens Expressway. Steel gates hide the windows of small plastics and metalworking shops. Nearby tenements are silent and dark. You’re wide awake, though, driving through the darkness on Kent Avenue, bumping over warped asphalt and steering around potholes. You’re circling Williamsburg, looking for the neighborhood that made Brooklyn cool. First you pass the Northside, the original center of Brooklyn’s hipster culture, a cluster of art galleries, cafés, bars, and boutiques around the subway station at North Seventh Street and Bedford Avenue. Then you pass the Southside, where French bistros and Japanese hair salons have recently joined yeshivas and bodegas, and artists and graduate students are a noticeable presence on the streets. Ahead of you stretch neighborhoods that have been predominantly black since after World War II but are now rapidly gentrifying and becoming socially and ethnically more diverse—that is, richer and whiter: Bedford-Stuyvesant, Fort Greene, Clinton Hill. The old Brooklyn Navy Yard sits vast and uninhabited just one block to the west. A few blocks beyond that, brownstone townhouses sell for a million dollars and up. Navigating solo through this dark landscape, you don’t see any sign of life. But when you turn onto the wider roadway of Flushing Avenue, you meet up with men and women walking in couples and groups of four. They are Hasidic Jews, women with heads covered in wigs and scarves, skirts below their knees, and black-hatted men wearing long black overcoats. Sabbath began at sundown. Because driving is prohibited then, any believers who are out on the street at this hour must find their way home on foot. After you pass the Hasidim, you find a few more people walking on the street; these men are wearing tight jeans and the women are in short skirts.
Union Square and the Paradox of Public Space
Authors: Zukin Sharon
Published: November 2020

At 6 o’clock on a weekday evening in early July, Union Square is most alive. The small, oval park at its center, three acres of green nestled between four broad streets, throbs with music and conversation, with voices rising and swelling to join the steady drone of traffic on all sides. You see children swinging under their parents’ eye in small playgrounds on the park’s northern edge; at the southern end you pick your way carefully through a swarm of a couple hundred young men and women who are milling around the wide, shallow stone steps leading up to the park’s main entrance. Tourists browse the T-shirt and art vendors’ tables while other shoppers stop at the Greenmarket on their way home, and every fifth person in the crowd is making a call or reading a text message on their cell phone. The crowd skews young, mostly under thirty-five, their faces are mainly white but also black and brown and several shades of tan, and you hear a girl ask, “Where are you? Are you in front?” in Japanese on her phone. Next to the subway entrance a lone political demonstrator uses a portable loudspeaker to make a speech against the U.S. president; nearby, under a statue of George Washington on horseback, two New York City police officers, also on horseback, interrupt their early evening patrol to chat with a park cleaner in a bright red uniform and a private security guard in navy pants and a matching cap. So many people are sitting on green wooden benches under the trees that you can hardly find two seats together. Most of the occupants are watching the parade of passersby; some are listening through earbuds to portable music players, others read a book, and one or two doze. In the fenced-in dog run, pets frisk about while their owners laugh and talk. A trio of young musicians sits on benches in the middle of the park, setting up a cello and two violins for an informal outdoor rehearsal.