bluuebunny/crossref_metadata_2025 huggingface dataset:
Clinical Presentation of Eyelid Lesions
Authors: Older J. Justin
Published: November 2020

Appropriate evaluation of an eyelid lesion is necessary before deciding on a course of surgical or nonsurgical treatment. A differential diagnosis is established based on the patient’s history and the physical characteristics of the mass. Many eyelid masses have similar physical and behavioral characteristics. In some cases, radiologic examination can be helpful in determining the extent or even the type of tumor. Certain malignant tumors may look benign or have the appearance of other malignancies. Biopsy is required for the definitive diagnosis. When faced with an eyelid lesion, the physician must first determine whether the lesion is benign or malignant. This determination will then dictate the next direction of diagnostic tests. If a mass has been present for several months to years or if there has been a history of bleeding, malignancy must be considered. Pain is usually not a component of malignancy, but some moderate discomfort may be present. Malignant lesions are usually destructive. The skin may be altered by a mass or ulceration. A malignancy located at the eyelid margin usually results in loss of lashes. Small malignancies may be similar in appearance to early inflammations, but as these malignancies grow, destruction of tissue is usually evident. If malignancy is not suspected, then a decision as to whether the lesion is inflammatory or not should be made. Small inflammatory lesions such as blepharitis may be ulcerative, cause loss of lashes, and simulate eyelid carcinoma. Swelling, redness, and pain are all characteristics of inflammatory masses such as styes or chalazia. Infected glands away from the lid margin can also have these signs. Swelling in the area of the medial canthus could be a lacrimal sac mucocele if there is no evidence of redness, or it could be a lacrimal sac tumor. Benign lesions that are not inflammatory may have swelling but usually not pain. They may be translucent, such as hair follicle cysts. These tumors often transilluminate. They may have a clear fluid that can be easily identified through thin skin, or there may be a yellowish content such as sebaceous material within the cyst. Some benign lesions may be papillomatous or have keratinized ends, such as cutaneous horns.
Management of Pediatric Nasolacrimal Duct Obstruction
Authors: Reddy Ashvini K. , Yen Kimberly G.
Published: November 2020

Tearing is a common presenting complaint in infants referred to an ophthalmologist and may be the first sign of something as benign as an impermanent anatomic defect or as grave as congenital glaucoma. When tearing is chronic, parents of an affected infant are often frustrated by the persistent accumulation of fluid and mucopurulent material in the eye and on the eyelids and anxious that the condition may be a sign of a more serious problem. The best initial management of tearing in an infant is to take a detailed history, which often provides important clues as to the cause of tearing, and then to perform a thorough, systematic ophthalmic examination. Tears serve four main functions: (1) they form a tear film to keep the eye moist, (2) they lubricate the eye, (3) they keep the eye clear of particulate matter and debris, and (4) they provide a refractive surface on the corneal epithelium. The tear film comprises three layers: a thin inner layer of proteinaceous mucin coats and protects the eye, an aqueous layer keeps the eye moist and lubricated, and an outer lipid layer slows evaporation of the aqueous layer. Basal tears are produced by the accessory lacrimal glands located in the conjunctiva and keep the eye moist under steady-state conditions; normal patients have a tear meniscus (or “tear lake”) visible along the inner lower eyelid as a result of basal tear production. Irritation or emotional extremes can trigger reflex tear production by the main lacrimal gland in the superotemporal quadrant of the orbit, “flooding” the tear lake. The level of the tear lake is highest when the rate of tear production by the lacrimal glands exceeds the rate of tear drainage into the nasolacrimal system. Tears normally drain out of the eye through puncta located on the nasal portion of the upper and lower eyelids. They then enter the upper and lower canaliculi, which run inferiorly and medially before joining to form the common canaliculus, which conducts tears through the valve of Rosenmuller and into the lacrimal sac.
Enucleation and Evisceration
Authors: Jordan David R. , Klapper Stephen R.
Published: November 2020

Loss of an eye to tumor, trauma, or end-stage ocular disease is devastating. There is a loss of binocular vision with a reduced peripheral visual field and loss of depth perception. Job limitations are often a result of lost binocularity, and affected individuals may experience a sense of facial disfigurement. Since eye contact is such an essential part of human interaction, it is extremely important for the artificial eye patient to maintain a natural, normal-appearing prosthetic eye. Characteristics of the ideal anophthalmic socket include: 1. A centrally placed, well-covered, buried implant of adequate volume, fabricated from a bioinert material 2. A socket lined with healthy conjunctiva and fornices deep enough to retain a prosthesis and to permit horizontal and vertical excursion of an artificial eye 3. Eyelids with normal position and appearance, as well as adequate tone to support a prosthesis 4. A supratarsal eyelid fold that is symmetric with the supratarsal fold of the contralateral eyelid 5. Normal position of the eyelashes and eyelid margin 6. Good transmission of motility from the implant to the overlying prosthesis 7. A comfortable ocular prosthesis that looks similar to the sighted, contralateral globe. Currently, no surgical procedure satisfies all the above requirements, as evidenced by the variety of surgical techniques advocated over the years. Over the past few decades, however, there have been numerous developments and refinements in anophthalmic socket surgery with respect to implant material and design, implant wrapping, implant–prosthesis coupling, and socket volume considerations. It is now more possible than ever to provide the anophthalmic patient with an artificial eye that looks and moves almost as naturally as a normal eye. As early as 500 b.c., Egyptian and Roman priests wore clay prostheses held in place with an adhesive substance or thong as external cosmetic coverings for disfigured and phthisical globes. Enucleation and evisceration techniques were not formally described in live patients until the late 16th century in Europe. Johannes Lange (1485–1565) made reference to removal of an eye, but George Bartisch in 1583 is credited with the first recorded description of removal of an eye for treatment of severe ocular disease.
Double Syndromes:Autism Associated with Genetic, Medical and Metabolic Disorders
Authors: Gillberg Christopher
Published: November 2020

A number of conditions—genetic, metabolic, and medical syndromes—have a high rate (more than expected by chance; i.e., more than a few percent) or a very high rate (more than 20%) of several autism symptoms associated with them. In the presence of these syndromes, the diagnosis of autistic disorder or autism spectrum disorder (ASD) is very often appropriate (Gillberg and Coleman 2000). These conditions are listed in Table 2.1. Some conditions, like Down syndrome, have a much lower rate of autistic symptoms than other of the listed syndromes, but, nonetheless, present a much higher rate than expected in the general population. A number of these syndromes are also discussed elsewhere in this volume, where the full range of cognitive and behavioral complications are addressed. Angelman syndrome is characterized by jerky movements, unprovoked laughter, and varying degrees of mental retardation, mostly severe or profound (Horsler and Oliver 2006). The rate of Angelman syndrome in the general population has been estimated at about 1 in 12,000 children, with a 1:1 male-to-female ratio (Steffenburg, Gillberg, Steffenburg, & Kyllerman 1996). Angelman syndrome (formerly known as ‘happy puppet syndrome’) is usually caused by a deletion of chromosome 15q11.2–12, which is similar, but not identical, to that found in children with Prader-Willi syndrome and is maternally, rather than paternally, inherited. The deletion includes a gene for the β-3 subunit of the γ-aminobutyric acid (GABA) receptor (Saitoh et al. 1994). Sixty to 75% of patients have deletions or rearrangements in the long arm of chromosome 15, and the deletion is always on the maternal chromosome. A small proportion of cases have paternal disomy for chromosome 15. At least 20% of affected persons have normal chromosomes and no evidence of disomy. In some of these cases, recurrence in relatives may be observed. Such cases may be due to a dominant mutation of the UBE3 gene at 15q11–13 resulting in an Angelman phenotype only when transmitted by females. Differences in clinical presentation are related to the nature of the genetic defect (Lossie et al. 2001).
Addison Disease
Authors: Rosebush Patricia I. , Anglin Rebecca E.
Published: November 2020

In 1855, Thomas Addison published a monograph in which he described 11 patients with adrenal disease (Addison 1855; Jeffcoate 2005). He emphasized their “general languor” and, in keeping with his interest in dermatological conditions, the “peculiar change” in skin color. This illness, caused by destruction of the adrenal cortex, has come to be known as Addison disease (AD). In this chapter, we begin by outlining the basic biology pertinent to an understanding of AD, followed by an outline of the clinical features of the illness and the etiological factors to be considered in children and adolescents presenting with AD. We then discuss the neuropsychiatric manifestations of AD and the mechanisms that can give rise to these. The adrenal glands, which sit on the upper poles of each kidney, are comprised of a number of distinct subregions, each of which is specialized for the synthesis and release of a particular hormone. The inner zona fasciculata of the adrenal cortex is responsible for the production and secretion of the glucocorticoid, cortisol, which participates in the hypothalamo-pituitary-adrenal (HPA) axis. The outer layer of the adrenal cortex, called the zona glomerulosa, produces the mineralocorticoid aldosterone, which is part of the renin-angiotensin system. The zona reticulata secretes the androgen dehydroepiandrosterone (DHEA), which is partially controlled by adrenocorticotropic hormone (ACTH) released from the pituitary. All three of these steroid hormones are affected in AD. The clinical signs and symptoms have traditionally been attributed to the deficiencies of cortisol and aldosterone, although recent evidence suggests that reduced levels of DHEA might play a role in the development of mood disturbances and the general loss of well-being in women with AD. The adrenal medulla, which secretes epinephrine and norepinephrine in response to stimulation from the sympathetic nervous system, is anatomically distinct from the cortex and not thought to be affected in AD (Hunt et al. 2000; Oelkers 1999). There is, however, compelling evidence of “cross-talk” or bidirectional interaction between these two parts of the adrenal gland (Bornstein and Chrousos 1999), both of which are critical components of the stress response.
Short Stature and the Relationship to Male Mental Health Status
Authors: Mobbs Elsie
Published: November 2020

Growth treatment for human growth failure when its cause is not identified is generally justified by two possible outcome measures: an increase in height and an increase in psychological well-being. An endocrinological cosmetic increase in height can arguably only be justified if it can be demonstrated as being likely to increase psychological well-being. New evidence is pointing to improved growth and mental health outcomes through psychotherapeutic family intervention during the child’s infancy. The medical definition of short stature (SS) is arbitrary (Cowell 1995): SS is usually defined for the height of an individual who is in less than the 3rd percentile of the reference range, which is 1.88 standard deviations (SDs) below the population mean (National Center for Health Statistics 1977; WHO 1986, 2006). Short stature may be caused by a multitude of factors, sometimes overlapping, and it may have many potential classifications. The condition of maturational delay occurs when significant SS and delayed pubertal development are seen in an otherwise healthy male (Cowell 1995; Cowell, Craig, and Ambler 1999; Cowell and Walker 1996). The medical diagnosis of maturational delay short stature (MDSS) is (a) considered in individuals with a late onset of puberty in which there is a family history of delayed puberty and an absence of organic symptoms or signs; and (b) diagnostic differentiation is made between MDSS and idiopathic short stature (ISS), with the latter encompassing MDSS but failing to meet the criteria of delayed puberty. When a history of SS is present in family members, the diagnosis of familial SS (FSS) is considered. Males present for treatment of SS much more frequently than females, which is a reflection of biology and possible societal bias, and some will present with behavioral disturbances. Multifactorial causes for these behavior problems can be embedded in past history and are not always easily accessible (Seegal 2000). Home environment problems may be present in growth failure, especially when demonstrated behavior problems are present (Gohlke et al. 1998; Nieves-Rivers et al. 1998).
Neurologic Aspects of the Smith-Magenis Syndrome
Authors: Gropman Andrea L. , Smith Ann C. M.
Published: November 2020

The Smith-Magenis syndrome (SMS) is a multiple congenital anomaly and mental retardation syndrome (Greenberg et al. 1996). The clinical phenotype includes distinctive craniofacial and skeletal features that change with age, a history of infantile hypotonia, significant expressive language delay, mental retardation, stereotypies, behavioral problems, and a sleep disorder (Potocki et al., 2000; De Leersynder et al. 2001). Two genetic mechanisms can cause SMS: an interstitial deletion involving chromosome 17p11.2 (including the retinoic acid–induced 1 [RAI1] gene) or a mutation in the RAI1 gene (Smith et al. 1986; Seranski et al. 2001; Slager et al. 2003). First described by Smith and colleagues in 1982, in two severely impaired patients (Smith et al. 1982), the phenotypic spectrum has been expanded by the recognition of additional cases (Smith et al. 1986; Stratton et al., 1986). The estimated prevalence of SMS deletion cases was reported to be 1 in 25,000 (Greenberg et al. 1991). However, new cases identified in the last decade as a result of improved molecular cytogenetic techniques (including microarray technology) now suggest the incidence to be closer to 1 in 15,000 births (Elsea and Girirajian 2008). Despite this improvement in technology accounting for new cases identified in the last several years, clinical diagnosis based on phenotypic recognition is often delayed. The phenotype of SMS becomes more pronounced and recognizable with advancing age both in terms of the physical and dysmorphic characteristics, as well as in the behavioral features (Gropman et al. 2006). Infants with SMS present with hypotonia, weak hoarse cry, decreased vocalization, and complacency (Gropman et al. 1998; 2006; Martin et al. 2006; Wolters et al.,2009). Gross and fine motor skill development is delayed in the first year of life. Sensory integration problems are frequently noted. Social skills are often age appropriate, delaying diagnosis in some cases. In older children, developmental delay, in particular expressive language delays, as well as emerging behavioral difficulties (Gropman et al. 2006; Martin et al. 2006; Madduri et al. 2006) and sleep disturbance may bring patients to clinical attention.
Tuberous Sclerosis Complex
Authors: Curatolo Paolo , D’Agati Elisa
Published: November 2020

Tuberous sclerosis complex (TSC) is a genetic, variably expressed, multisystem disorder that can cause circumscribed, benign, noninvasive lesions in any organ (Curatolo 2003; Gomez 1999). It affects about 1 newborn in every 6000 (Osborne, Fryer et al. 1991). The term tuberous sclerosis of the cerebral convolutions was used more than a century ago to describe the distinctive findings at autopsy in some patients with seizures and mental subnormality; the term tuberous describes the potato-like consistency of gyri with hypertrophic sclerosis (Bourneville 1880). The wide range of organs affected by the disease implies an important role for the TSC1 and TSC2 genes encoding hamartin and tuberin in the regulation of cell proliferation and differentiation. Tuberous sclerosis complex is a protean disease: the random distribution, number, size, and location of lesions cause varied clinical manifestations, involving the brain, skin, eyes, heart, kidney, lung (Curatolo et al. 2008). Some lesions, such as renal angiomyolipomas, do not occur until a certain age; by contrast, cardiac rhabdomyomas appear in the fetus and almost always regress spontaneously in infancy (Sosunov et al. 2008). About 85% of children and adolescents with TSC have central nervous system (CNS) manifestations, including epilepsy, learning difficulties, mental retardation, challenging behavioral problems, autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD), which can be associated with the structural CNS features generally seen in TSC (Curatolo et al. 1991; Gillberg et al. 1994). Abnormalities of neuronal migration and cellular differentiation, and excessive cell proliferation, all contribute to the formation of the various TSC brain lesions including cortical tubers, subependymal nodules (SENs), subependymal giant cell astrocytomas (SEGAs), and widespread gray and white matter abnormalities, these latter being identified even in patients with average intelligence (Ridler et al. 2001; de Vries et al. 2005; Ridler et al. 2007). Further characterization of these typical lesions has been provided by progress in structural and functional imaging (DiMario 2004; Luat et al. 2007). Major and minor criteria exist to diagnose TSC (Table 32.1). The diagnosis is made when two major features, or one major and two minor ones, can be detected.
Myotonic Dystrophy
Authors: Winblad Stefan , Ekström Anne-Berit
Published: November 2020

The myotonic dystrophies, type 1 (DM1) and 2 (DM2) are progressive, autosomal, dominantly inherited disorders, mainly characterized by muscle weakness and atrophy but also by a variable impact on heart, eye, brain, and the endocrine and the gastrointestinal system (Meola 2000). The worldwide prevalence is approximately 1 in 8,000. They are considered to be most common in Western Europe and Japan, but less prevalent in Southeast Asia, and rare or absent in southern and central Africa (Emery 1991). A prevalence of 18 in 340,000 children has been reported (Darin and Tulinius 2000). The cause of myotonic dystrophies is an unstable inherited repeat DNA expansions. Expansions are elements occurring and repeated throughout the human genome, typically polymorphic in the general population. Repeats can become unstable during DNA replication and, depending on specific repeat motif and location, expanded repeats can become pathogenic. In disease states, the number of repeats exceeds the normal range, leading to various pathogenic mechanisms (Ranum and Cooper 2006). DM1 is associated with an expanded (CTG)n repeat (>50 to several thousands) within the noncoding 3′ untranslated region of the myotonic dystrophy protein kinase (DMPK) gene on chromosome 19q13.3. In DM2, another mutation exists, namely an expanded CCTG tetranucleotide repeat (from 75 to 11,000 repeats) in the first intron of the zinc finger protein 9 (ZNF9) gene on chromosome 3q21 (Day and Ranum 2005). This means that two unrelated genes are associated with similar phenotypes although there are differences, including the age of onset and severity of symptoms (Meola 2000). The first signs of a DM2 disease are typically shown in adulthood, and no study has as yet systematically described cognitive or behavioral abnormalities in a childhood DM2 phenotype. Consequently, the following chapter focuses on a description of DM1. In this disorder, the age of onset is variable, meaning that there are congenital cases, as well as children, adults and patients experiencing the first symptoms very late in life. DM1 is traditionally divided into categories, each presenting with specific clinical features and broadly associated with the age of onset and extent of genetic abnormality.
Cognitive and Behavioral Complications of Deafness
Authors: Wright Barry
Published: November 2020

The prevalence of profound deafness in the United Kingdom is reported as 9 per 10,000 in 3-year-olds to 16 per 10,000 in 9- to 16-year-olds, although it is estimated that these figures may be higher because of possible under-diagnosing (Fortnum et al. 2001). In England and Scotland, approximately 13 in 10,000 children have a permanent hearing impairment of 40 dB or more (moderate to profound) across the frequencies 500–4,000 Hz (Fortnum and Davis, 1997; Fortnum, 2003; Kennedy and McCann, 2008; MacAndie et al. 2003) and in 11 in 10,000 this loss is congenital. The remainder are acquired or progressive. Profound impairment (≥95 dB loss) occurs in 2.4 per 10,000. Bilateral sensorineural deafness had a prevalence of 21 per 10,000 in a Finnish birth cohort (1974–1987) (Vartiainen, Kemppinen, and Karjalainen 1997). A survey in the general population in Sichuan, China, found a prevalence of 1.9 per 1,000 profound deafness (Liu et al. 1993). Table 44.1 shows the World Health Organization (WHO) and British Society of Audiology definitions of degrees of deafness. Sensorineural deafness involves problems either in hair cell function in the cochlear or in the nerve transmission of sound. For bilateral sensorineural deafness, the diagnosis is made at variable ages in health systems in which there is no universal neonatal screening. This varies across cultures, but can still be surprisingly late even in modern health systems. One study of 106 children with bilateral sensorineural deafness showed a mean age for first diagnosis at 42 months (median 33 months) of age, with a range from 4 months to 11 years of age (Walch 2003). In another study in Glasgow, Scotland (Chaurasia and Geddes, 2008), only 50% of early childhood deafness presented before 2 years of age. Conductive deafness involves problems with sound travelling from the outer ear, through the middle ear, to the cochlear. The commonest cause is otitis media (“glue ear”), with losses usually in the mild to moderate range. About half of children between 2 and 4 years will have at least one episode of otitis media with effusion (OME) (Zielhuis, Rach, and Van den Brock 1990).
Neurobiological, Cognitive, and Behavioral Consequences of Child Maltreatment
Authors: Pears Katherine C. , Bruce Jacqueline
Published: November 2020

Child maltreatment is a serious public pediatric health problem that affected 900,000 children between the ages of 0 and 18 years in 2006; more than 1,500 of these children died as a result of abuse and neglect (United States Department of Health and Human Services [USDHHS] 2008). Survivors of maltreatment face cognitive, academic, social, and mental health consequences that may continue into adulthood (Springer et al. 2007; Widom et al. 2007). One recent study found that the mental health consequences of maltreatment were still apparent up to 40 years later (Springer et al. 2007). In addition to these human costs, the economic costs of maltreatment are high: approximately $103.8 billion in 2007, at least $6.6 billion of which was attributed to hospitalization alone (Wang and Holton 2007). The majority of child maltreatment occurs between the ages of 0 and 7 years, a period of extensive growth in the physical, cognitive, behavioral, and social domains, which might help to explain its long-lasting consequences. The highest rate of victimization occurs in children under the age of 1 year (24.4 per 1,000 children in 2006), followed by children between the ages of 1 and 3 years (14.2 per 1,000) and between 4 and 7 years (13.5 per 1,000; USDHSS 2008). Victimization rates decrease across the ages of 8–17 years. Boys and girls are almost equally likely to be victims of maltreatment; in 2006, 48% of children who were maltreated were boys (52% girls). Ethnic minority children are at the highest risk for maltreatment, with African American children, Native American/Alaska Native children, and children of multiple ethnicities showing the highest rates of maltreatment (19.8, 15.9, and 15.4 per 1,000 children of the same ethnic groups, respectively). It should be noted that all of these rates are based on reports of maltreatment and, thus, cannot account for maltreatment that is not reported to authorities. Another potential reason that the effects of child maltreatment might be long-lasting (and varied) is that maltreatment is not a homogenous experience.
Writing the Methods Section
Authors: Robinson Marin S , Stoller Fredricka L , Constanza-Robinson Molly , Jones James K
Published: November 2020

In this chapter, we focus on writing a Methods section for a journal-quality paper. We begin with the Methods section because this is the section that many chemists write first, in part because this section describes what they know best: the procedures they have repeated (many times) to conduct their work. Moreover, most research groups use similar methodologies for several years; hence, previously written Methods sections can serve as models for writing new Methods sections. Together, these factors make the Methods section one of the easier sections to write and an excellent place to begin our writing instruction. By the end of this chapter, you will be able to do the following: ■ Know how to address the intended audience of a Methods section ■ Recognize which details to include and exclude from a Methods section ■ Organize a Methods section following standard moves ■ Use capitalization, abbreviations, and parentheses appropriately ■ Format numbers and units correctly ■ Use verb tense and voice in conventional manners As you work through the chapter, you will write a Methods 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: 3A Read the literature 3B Describe materials 3C Describe experimental methods 3D Describe numerical methods 3E Practice peer review 3F Fine-tune your Methods section The purpose of the Methods section is to address how a particular work was conducted. Relevant information about instrumentation and experimental and/ or numerical procedures is described. The goal is to describe the information in enough detail that an expert (not a novice) could repeat the work. Usually, this section is formally called, for example, Materials and Methods or Experimental Section, but for brevity, we call it simply the Methods section. Many of you have written a Methods section previously for a college-level chemistry course. Thus, we begin with an exercise to test your current knowledge about writing a Methods section.
Geography of Jeopardy
Authors: De Blij Harm
Published: November 2020

Everyone lives with risk, every day. In the United States, more than 100,000 persons die from accidents every year, nearly half of them on the country’s roads. Worldwide, an average of more than 5000 coal miners perish underground annually, a toll often forgotten by those who oppose nuclear power generation on grounds of safety. From insect bites to poisoned foods and from smoking to travel, risk is unavoidable. Certain risks can be mitigated through behavior (not smoking, wearing seatbelts), but others are routinely accepted as inescapable. A half century ago, long before hijackings and airport security programs, the number of airline travelers continued to increase robustly even as airplanes crashed with considerable frequency. Today, few drivers or passengers are deterred by the carnage on the world’s roads, aware of it though they may be. Risk is part of life. Risk, however, also is a matter of abode, of location. Who, after experiencing or witnessing on television the impact of a hurricane, a tornado, an earthquake, a volcanic eruption, a flood, a blizzard, or some other extreme natural event, has not asked the question: “Where in the world might be a relatively safe place to live?” Geographers, some of whom have made the study of natural hazards and their uneven distribution a research priority, don’t have a simple answer. But on one point they leave no doubt: people, whether individually or in aggregate, subject themselves to known environmental dangers even if they have the wherewithal to avoid them. Many Americans build their retirement or second homes on flood-prone barrier islands along coastlines vulnerable to hurricanes. The Dutch, who have for many years been emigrating from the Netherlands in substantial numbers, are leaving for reasons other than the fact that two-thirds of their country lies below sea level. From Indonesia to Mexico, farmers living on the fertile slopes of active volcanoes not only stay where they are, but often resist even temporary relocation when volcanic activity resumes. From Tokyo to Tehran, people continue to cluster in cities with histories of devastating earthquakes and known to be situated in perilous fault zones. Fatalism is a cross-cultural human trait.
Measuring Chemical Quantities: The Mole
Authors: Oriakhi Christopher O.
Published: November 2020

A mole is defined as the amount of a given substance that contains the same number of atoms, molecules, or formula units as there are atoms in 12 g of carbon-12. For example, one mole of glucose contains the same number of glucose molecules as there are carbon atoms in 12 g of carbon-12. The number of atoms in exactly 12 g of carbon-12 has been determined to be 6.02×1023. This number, 6.02×1023, is called Avogadro’s number (NA). Therefore, a mole is the amount of a substance that contains Avogadro’s number of atoms, ions, molecules, or particles. For example: 1 mol He atoms = 6.02×1023 atoms 1 mol CH3 OH molecules = 6.02×1023 molecules 1 mol SO2−4 ions = 6.02×1023 ions The term molar mass is now commonly used as a general term for both formula mass and molecular mass. The molar mass of any substance is the mass in grams of one mole of the substance, and it is numerically equal to its formula mass (expressed in amu). For example, the formula mass of glucose, C6H12O6, is 180.0 amu. So the molar mass or the mass in grams of 1 mol of glucose is 180.0 g. In terms of chemical arithmetic, the mole is the most important number in chemistry. It provides useful stoichiometric information about reactants and products in any given chemical reaction. The quantities commonly encountered in chemical problems include the number of moles of a substance; the number of atoms, molecules, or formula units of a substance; and the mass in grams. These quantities are related and can be readily interconverted with the aid of the molar mass and Avogadro’s number. Calculations based on the mole can be carried out by using conversion factors, or with simple equations based on the conversion factor.
Oxidation and Reduction Reactions
Authors: Oriakhi Christopher O.
Published: November 2020

Oxidation-reduction reactions, or redox reactions, occur in many chemical and biochemical systems. The process involves the complete or partial transfer of electrons from one atom to another. Oxidation and reduction processes are complementary. For every oxidation, there is always a corresponding reduction process. This is because for a substance to gain electrons in a chemical reaction, another substance must be losing these electrons. Oxidation is defined as a process by which an atom or ion loses electrons. This can occur in several ways: • Addition of oxygen or other electronegative elements to a substance:. . . 2 Mg(s)+O2(g) → 2 MgO(s) . . .2 Mg(s)+O2(g) → MgCl2 (s). . . • Removal of hydrogen or other electropositive elements from a substance: . . . H2S(g)+Cl2(g) → 2 HCl(g)+S(s) . . .Here, H2S is oxidized. • The direct removal of electrons from a substance: . . . 2 FeCl2 (s)+Cl2(g) → 2 FeCl3 (s) . . . Fe2+ → Fe3+ +e− . . . Reduction is defined as the process by which an atom or ion gains electrons. This can occur in the following ways: • Removal of oxygen or other electronegative elements from a substance: . . . MgO(s)+H2(g) → Mg(s)+H2O(g). . . • Addition of hydrogen or other electropositive elements to a substance: . . . H2(g)+Br2(g) → 2 HBr(g). . . 2 Na(s)+Cl2(g) → 2 NaCl(s). . . Here, chlorine (Cl2) is reduced. • The addition of electrons to a substance: . . . Fe3+ +e− → Fe2+ . . . Oxidation number or oxidation state is a number assigned to the atoms in a substance to describe their relative state of oxidation or reduction. These numbers are used to keep track of electron transfer in chemical reactions. Some general rules are used to determine the oxidation number of an atom in free or combined state. 1. Any atom in an uncombined (or free) element (e.g., N2, Cl2, S8, O2, O3, and P4) has an oxidation number of zero. 2. Hydrogen has an oxidation number of +1 except in metal hydrides (e.g., NaH, MgH2) where it is −1. 3. Oxygen has an oxidation number of −2 in all compounds except in peroxides (e.g., H2O2, Na2O2) where it is –1.
Do Your Job
Authors: Fish Stanley
Published: November 2020

So back to the basic question. What exactly is the job of someone who teaches in a college or a university? My answer is simple and follows from legal theorist Ernest Weinrib’s account of what is required if an activity is to have its own proper shape. It must present itself “as a this and not a that.” As I have already said, the job of someone who teaches in a college or a university is to (1) introduce students to bodies of knowledge and traditions of inquiry they didn’t know much about before; and (2) equip those same students with the analytical skills that will enable them to move confidently within those traditions and to engage in independent research should they choose to do so. Job performance should be assessed on the basis of academic virtue, not virtue in general. Teachers should show up for their classes, prepare lesson plans, teach what has been advertised, be current in the literature of the field, promptly correct assignments and papers, hold regular office hours, and give academic (not political or moral) advice. Researchers should not falsify their credentials, or make things up, or fudge the evidence, or ignore data that tells against their preferred conclusions. Those who publish should acknowledge predecessors and contributors, provide citations to their sources, and strive always to give an accurate account of the materials they present. That’s it, there’s nothing else, and nothing more. But this is no small list of professional obligations, and faculty members who are faithful to its imperatives will have little time to look around for causes and agendas to champion. A faculty committee report submitted long ago to the president of the University of Chicago declares that the university exists “only for the limited . . . purposes of teaching and research” and reasons that “since the university is a community only for those limited and distinctive purposes, it is a community which cannot take collective action on the issues of the day without endangering the conditions for its existence and effectiveness” ( Kalven Committee Report on the University’s Role in Political and Social Action, November 11, 1967).
Don’t Try to Do Someone Else’s Job
Authors: Fish Stanley
Published: November 2020

Some of the hits taken by administrators will be delivered by those faculty members who have forgotten (or never knew) what their job is and spend time trying to form their students’ character or turn them into exemplary citizens. I can’t speak for every academic, but I am not trained to do these things, although I am aware of people who are: preachers, therapists, social workers, political activists, professional gurus, inspirational speakers. Teachers, as I have said repeatedly, teach materials and confer skills, and therefore don’t or shouldn’t do a lot of other things—like produce active citizens, inculcate the virtue of tolerance, redress injustices, and bring about political change. Of course a teacher might produce some of these effects—or their opposites—along the way, but they will be, or should be, contingent and not what is aimed at. The question that administrators often ask, “What practices provide students with the knowledge and commitments to be socially responsible citizens?” is not a bad question, but the answers to it should not be the content of a college or university course. No doubt, the practices of responsible citizenship and moral behavior should be encouraged in our young adults, but it’s not the business of the university to do so, except when the morality in question is the morality that penalizes cheating, plagiarizing, and shoddy teaching. Once we cross the line that separates academic work from these other kinds, we are guilty both of practicing without a license and of defaulting on our professional responsibilities. But isn’t it our responsibility both as teachers and as citizens to instill democratic values in our students? Derek Bok thinks so and invokes studies that claim to demonstrate a cause and effect relationship between a college education and an active participation in the country’s political life: “researchers have shown that college graduates are much more active civically and politically than those who have not attended college” (Our Underachieving Colleges). But this statistic proves nothing except what everyone knows: college graduates have more access to influential circles than do those without a college education.
Social Anxiety Disorder (Social Phobia)
Authors: Starcevic, MD, PhD Vladan
Published: November 2020

Social anxiety disorder (SAD) is conceptualized as an excessive and/or unreasonable fear of situations in which the person’s behavior or appearance might be scrutinized and evaluated. This fear is a consequence of the person’s expectation to be judged negatively, which might lead to embarrassment or humiliation. Typical examples of feared and usually avoided social situations are giving a talk in public, performing other tasks in front of others, and interacting with people in general. Although the existence of SAD as a psychopathological entity has been known for at least 100 years, it was only relatively recently, with the publication of DSM-III in 1980, that SAD (or social phobia) acquired the status of an ‘‘official’’ psychiatric diagnosis. The term social anxiety disorder has been increasingly used instead of social phobia, because it is felt that the use of the former term conveys more strongly the pervasiveness and impairment associated with the condition and that this term will promote better recognition of the disorder and contribute to better differentiation from specific phobia (Liebowitz et al., 2000). Like generalized anxiety disorder, social anxiety disorder is common and controversial. Unlike generalized anxiety disorder, which is described in different ways by different diagnostic criteria and different researchers and clinicians, SAD does not suffer from a ‘‘description problem.’’ It is not particularly difficult to recognize features of SAD; what may be difficult is making sense of these features. Main issues associated with SAD are listed below…. 1. Where are the boundaries of SAD? How well is SAD distinguished from ‘‘normal’’ social anxiety and shyness on one hand, and from severe psychopathology on the other? 2. Is there a danger of ‘‘pathologizing’’ intense social anxiety by labeling it a psychiatric disorder? How can the distress and suffering of people with high levels of social anxiety be acknowledged if they are not given the corresponding diagnostic label? 3. Is SAD a bona fide mental disorder? 4. Can the subtyping scheme (nongeneralized vs. generalized SAD) be supported? 5. Is there a spectrum of social anxiety disorders?
Posttraumatic Stress Disorder
Authors: Starcevic, MD, PhD Vladan
Published: November 2020

Posttraumatic stress disorder (PTSD) develops in predisposed individuals who have had a traumatic experience. There are many different ways in which PTSD presents itself, and only some of them(e.g., avoidance behavior, symptoms of hyperarousal)make it look like other anxiety disorders. Various manifestations of PTSD have led to its also being considered primarily a disorder of memory, a dissociative disorder, or a condition more closely related to depression. Given the presumed etiological link between a traumatic event and PTSD, there is a rare opportunity among psychiatric disorders for implementation of strategies that might prevent the development of PTSD. Most people recover after trauma, while many of those who do develop PTSD remit spontaneously. Still, a proportion of traumatized people develop a chronic form of PTSD–a condition that is often very difficult to treat. Posttraumatic stress disorder has been a controversial entity since its official introduction in the psychiatric classification in 1980.Anumber of issues have arisen, and many of them remain unresolved. Some of the key questions are listed below…. 1. Is the concept of PTSD too heterogeneous? 2. Are there different types of PTSD or different disorders arising in the aftermath of trauma? 3. Has the concept of a traumatic event become too broad? Alternatively, can a greater variety of stressful events precipitate PTSD? 4. Is the occurrence of trauma necessary for the development of PTSD? 5. Are there any specific or unique features of PTSD, which would allow its differentiation from related disorders? 6. Has the concept of PTSD been overused or misused, especially in the context of compensation claims and litigation? Does PTSD reflect a ‘‘medicalization’’ of the normal human reactions and emotions in response to trauma? 7. What accounts for the fact that the majority of trauma victims recover spontaneously from early PTSD-like symptoms, whereas some go on to develop a chronic, severe, and debilitating PTSD? Has there been too much emphasis on vulnerability to developing post-trauma psychopathology and too little attention paid to factors such as resilience? 8. Why do we still have a difficulty understanding what combination of risk factors best predicts the development of PTSD?
Early Warning Signs and Preventing a Relapse
Authors: Compton Michael T , Broussard Beth
Published: November 2020

In this chapter, we discuss early warning signs, which are signs and symptoms that often occur before an episode of psychosis. These signs and symptoms, though mild, may occur before the first episode of psychosis and also before later episodes. That is, some mild signs and symptoms may occur during the prodromal phase of the illness, before psychotic symptoms first develop. These same signs and symptoms often serve as warning signs before another episode of illness, or a relapse of psychosis, occurs. So, it is important to be familiar with early warning signs and what to do if they begin to develop. Many people who have had a first episode of psychosis will go on to have one or more relapses of their illness. A relapse happens when symptoms appear again. Some relapses may happen with little or no warning over a short period of time, such as a few days. However, most relapses develop slowly over longer periods, like a few weeks. A relapse may or may not require hospitalization, but it definitely calls for immediate attention, evaluation, and treatment. After a stay in the hospital or after outpatient stabilization, some people feel better quickly. Others take weeks, or even months, to function as well as they had before the relapse. One way of avoiding a relapse is to stay in treatment and attend all follow-up appointments (see Chapter 8 on Follow-up and Sticking with Treatment). Also, it is very important to become aware of one’s specific early warning signs, which are changes in thoughts, feelings, and behaviors that happen a few days or weeks before an episode (reappearance of symptoms). By carefully watching for these signs, patients, their families, and their mental health professionals can work together to help lessen the severity of any episode that may occur. Relapse prevention is the goal of preventing a relapse altogether, by sticking to treatment and watching for early warning signs. The first step in determining one’s specific early warning signs is to think back to the changes that occurred in the prodromal period of the illness, or the time just before the first episode of psychosis. While there are common early warning signs, they will show up slightly differently in each person. Early warning signs in one person may be clear and easy to detect, while in another person they may be trickier to figure out. Early warning signs are signals that symptoms are beginning again and that another episode of psychosis may happen.
HIV, AIDS, and Medical Multimorbid Illnesses
Authors: Lux Joseph Z. , Goforth Harold W.
Published: November 2020

Since the introduction of combination antiretroviral therapy, clinicians have seen a sharp decrease in the incidence of many HIV-associated comorbidities, and patients with access and adherence to combination antiretroviral therapy are living longer and healthier lives. However, the frequency of endocrine, metabolic, cardiovascular, renal, dermatological, neoplastic, hepatic, renal, pulmonary, and gastrointestinal multimorbid medical conditions remains very significant and in some cases is increasing. Although the incidence of particular HIV-associated comorbidities such as cytomegalovirus (CMV) retinitis has declined considerably, it remains a significant source of distress and suffering for persons with AIDS. This chapter is not intended to provide a lengthy discourse on each topic addressed, but rather be a general overview that will give the reader a basic working knowledge of multimorbid medical conditions and enhance the understanding of associated psychiatric complications and psychological distress. For a summary of these conditions and their respective features and treatment, see Table 10.1. HIV and AIDS have been associated with a wide spectrum of endocrine abnormalities that underscore the complex relationships between immunological, endocrinological, and psychological systems. Endocrinopathies are great mimickers of psychiatric disorders, manifesting in some cases as disturbances of mood, sleep, appetite, thought process, energy level, or general sense of well-being. Endocrinopathies may present insidiously or abruptly, in either case with potentially tragic consequences when misdiagnosed as psychopathology. Prompt recognition of reversible alterations in endocrine function is essential to prevent unnecessary morbidity and mortality. An understanding of the complex interactions between endocrine and psychological systems may improve recognition and treatment of endocrinopathies, diminish suffering, and enhance quality of life and longevity in persons with HIV and AIDS. Many studies have demonstrated alterations in adrenal function in patients with HIV and AIDS. Associated infections and tumors, as well as direct invasion of the adrenal glands by the virus, partly explain these changes. Patients are also commonly prescribed drugs that alter steroid synthesis or metabolism; for example, ketoconazole decreases steroid synthesis, megesterol acetate suppresses pituitary secretion of corticotropin, and rifampin increases p450 activity, leading to increased metabolism of cortisol.