bluuebunny/crossref_metadata_2025_split huggingface dataset:
Angiostrongyliasis
Authors: Knight Richard 
Published: February 2020

Abstract
The rat lungworm Angiostrongylus cantonensis causes outbreaks of eosinophilic meningitis in parts of Southeast Asia, East Asia, Oceania, and the Caribbean. Human infections follow ingestion of raw snails (the primary intermediate hosts), food contaminated by snail mucus, or one of several paratenic hosts. Clinical manifestations include headache, meningism, vomiting, cranial nerve, ocular, lesions, and rarely seizures. Lumbar puncture reveals eosinophilic meningitis and sometimes larval worms. Treatment is usually with prednisolone alone, or with albendazole and prednisolone. Mortality is usually below 2%. Prevention is by avoidance of raw high-risk dietary items and unwashed salads. Another species A. costaricensis causes granulomatous bowel and hepatic lesions in some tropical American countries. Rats are the definiitive hosts, human infection follows ingestion of small slugs. Treatment is surgical.
Diseases of high terrestrial altitudes
Authors: Albert Tyler , Swenson Erik R. , Pollard Andrew J. , Basnyat Buddha , Murdoch David R. 
Published: February 2020

Abstract
Ascent to altitudes above 2,500 m leads to exposure to hypobaric hypoxia. This affects performance on first arrival at high altitude and disturbs sleep, but physiological changes occur over time to defend arterial and tissue oxygenation and allow the individual to adjust. This process of acclimatization includes (1) an increase in the rate and depth of breathing; and (2) an increase in red cell mass, and in red cell 2,3-diphosphoglycerate. Acclimatization is no longer possible at extreme altitude (&gt;5,800 m) and the exposed individual will gradually deteriorate. Altitude illness results from a failure to adjust to hypobaric hypoxia at altitude. Risk is increased by ascent to higher altitudes, by more rapid gain in altitude, and (in some people) genetic predisposition; the condition may be avoided in most cases by slow, graded ascent.
Bioterrorism
Authors: Green Manfred S. 
Published: February 2020

Abstract
Bioterrorism is the deliberate use of biological agents to cause illness, death, and fear for ideological or personal purposes. The agents might be disseminated through aerosolization, food, human carriers, infected insects, or water. The incubation periods of these agents can vary from hours to weeks, with early symptoms mimicking many other infectious diseases. The diagnosis might not be suspected unless cases occur in clusters. Early identification of outbreaks will depend largely on the ability of primary care and emergency room physicians to identify and promptly report cases to the public health authorities. Specific treatment (if available) of affected individuals will depend on the pathogen, and for contagious diseases such as smallpox and plague, isolation of patients and their contacts, barrier nursing, quarantine, and restriction of the movements and social interactions of people are important control measures.
Obesity
Authors: Farooqi I. Sadaf 
Published: February 2020

Abstract
Obesity is defined as an excess of body fat that is sufficient to affect health adversely. While the quantification of fat mass is usually only performed in the research setting, body mass index (weight in kg/height in metres2) is a useful surrogate marker for fat mass. Using the World Health Organization definition of a body mass index more than 30 kg/m2 to define obesity, 30% of Americans and 10–20% of Europeans are classified as obese, with the prevalence rising in many developing countries. As body mass index increases, so does the relative risk of type 2 diabetes, hypertension, and cardiovascular disease. As such, obesity is associated with disability, mortality, and substantial health costs. At an individual level, severe obesity can be associated with sleep disturbance and respiratory difficulties, joint and mobility disorders, as well as considerable social stigma which can affect quality of life, educational attainment, and employment opportunities.
Disorders of purine and pyrimidine metabolism
Authors: Marinaki Anthony M. , Fairbanks Lynette D. , Watts Richard W.E. 
Published: February 2020

Abstract
Disorders of purine and pyrimidine metabolism are due to abnormalities in the biosynthesis, interconversion, and degradation of the purines—adenine and guanine—and of the pyrimidines—cytosine, thymine, and uracil. The purine nucleotides, their cyclic derivatives (cAMP and cGMP), and their more highly phosphorylated derivatives have functions in many aspects of intermediary metabolism. Purine compounds also function as signal transducers, neurotransmitters, vasodilators, and mediators of platelet aggregation. Disorders of purine metabolism—the end point of purine metabolism in humans is uric acid. When uric acid levels become supersaturated in body fluids, uric acid and sodium urate monohydrate crystallize, causing gout. This results from either overproduction or underexcretion of urate, or from a combination of these defects. Decreased net tubular urate secretion is most often due to genetic polymorphism in uric acid transporters and is the commonest cause of primary (‘idiopathic’) gout. Gout may be secondary to a wide variety of renal disorders. Gout is also a consequence of enzymatic defects that accelerate de novo purine synthesis. Acute attacks of gout are treated with nonsteroidal anti-inflammatory drugs, colchicine, or steroids. Hypouricaemia may be caused by inherited disorders of uric acid biosynthesis or may be due to inherited or acquired renal tubule transport defects. Disorders of pyrimidine metabolism—the de novo synthesis of pyrimidine nucleotides involves a series of six reactions beginning with the formation of carbamyl phosphate and concluding with orotidine monophosphate, which then undergoes a series of interconversion and salvage reactions. The inherited disorders of pyrimidine metabolism, which can present in a wide variety of ways, are much less common and/or much less easily recognized than disorders of purine metabolism.
Hereditary disorders of oxalate metabolism: The primary hyperoxalurias
Authors: Fargue Sonia , Milliner Dawn S. , Danpure Christopher J. 
Published: February 2020

Abstract
Primary hyperoxalurias (PHs) are rare inherited disorders characterized by an increased endogenous synthesis of oxalate caused by a deficiency in one of several liver and kidney enzymes involved in glyoxylate metabolism. The excess oxalate is eliminated from the body by the kidneys. High concentrations of oxalate in the urine increase the risk of calcium oxalate deposition in the kidney (resulting in nephrocalcinosis) and in the urinary tract (leading to urinary stones). Primary hyperoxaluria is characterized by recurring calcium oxalate stones, presenting from early childhood to late adult life. Over time, deposition of calcium oxalate crystals in kidney tissue leads to kidney damage with progressive loss of kidney function. Primary hyperoxaluria type 1 is the most severe form with a median age at end-stage renal failure reached during young adulthood. Patients with PH type 2 and PH type 3 may show preservation of kidney function well into adulthood. Systemic deposition of calcium oxalate (oxalosis) can follow kidney failure and increased plasma oxalate levels. Diagnosis is made by DNA analysis of peripheral blood samples, or more rarely by enzyme assay of liver biopsy tissue. Treatment relies on high fluid intake, inhibitors of calcium oxalate crystallization, and, when required, urological procedures for stone removal. Some patients with PH1 respond to vitamin B6 treatment. Management of end-stage renal failure is difficult as dialysis, whether haemo- or peritoneal, cannot match oxalate production. Isolated kidney transplantation places patients at risk of recurring oxalate deposition in the graft in PH1 patients not responsive to vitamin B6. Liver transplantation, usually combined with kidney transplantation, is a curative treatment for PH1 but carries significant risks.
Principles of hormone action
Authors: Fowkes Rob , Chatterjee V. Krishna , Gurnell Mark 
Published: February 2020

Abstract
Hormones, produced by glands or cells, are messengers which act locally or at a distance to coordinate the function of cells and organs. Types of hormone include: peptides (e.g. hypothalamic releasing factors) and proteins (e.g. insulin, growth hormone)—these generally interact with membrane receptors located on the cell surface, causing activation of downstream signalling pathways leading to alteration in gene transcription or modulation of biochemical pathways to effect a physiological response; steroids (e.g. cortisol, progesterone, testosterone, oestradiol) and other lipophilic substances (e.g. vitamin D, retinoic acid, thyroid hormone)—these act by crossing the plasma membrane to interact with intracellular receptors, with hormone action via nuclear receptors altering cellular gene expression directly.
Disorders of the posterior pituitary gland
Authors: Karavitaki Niki , Ahmed Shahzada K. , Wass John A.H. 
Published: February 2020

Abstract
The posterior pituitary produces arginine vasopressin, which has a key role in fluid homeostasis, and oxytocin, which stimulates uterine contraction during birth and ejection of milk during lactation. Cranial diabetes insipidus is the passage of large volumes of dilute urine due to vasopressin deficient synthesis and/or release. The most common cause is lesions of the neurohypophysis or the hypothalamic median eminence damaging the magnocellular neurons. MRI of the neurohypophysis is required to delineate the cause. Mild polyuria can be managed simply by ensuring adequate fluid intake; treatment with the long-acting vasopressin analogue, desmopressin is used for more severe cases. The syndrome of inappropriate antidiuresis is diagnosed when there is hyponatraemia with hypotonic plasma, inappropriate urine osmolality, and urinary sodium more than 20 mmol/litre, together with no evidence of volume overload or hypovolaemia, and normal renal, adrenal, and thyroid function.
Disorders of male reproduction and male hypogonadism
Authors: Bouloux P.-M.G. 
Published: February 2020

Abstract
The adult testis performs two principle functions: the synthesis and secretion of androgens, and the production of male germ cells, the spermatozoa. Testosterone is essential for male sexual differentiation, growth, and function of the male genital tract, secondary sexual characteristics, sexual potency, and production of spermatozoa. Hypogonadism may be due to disorders of the pituitary/hypothalamus (secondary or hypogonadotropic hypogonadism) or testes (primary or hypergonadotropic hypogonadism). Its symptoms and signs depend on the age of onset of androgen deficiency. Prepubertal presentation is with sexual infantilism, delayed puberty, and eunuchoidal body proportions. Male infertility may affect 5% of men of reproductive age and is caused by a heterogeneous group of disorders. The commonest cause (60% of cases) is ‘idiopathic’ azoo/oligozoospermia, although many cases are now recognized as due to discrete gene defects associated with impaired spermatogenesis. Other causes include cryptorchidism, testicular tumours, genital tract infection, obstructive azoospermia, and sperm autoimmunity.
Sexual dysfunction
Authors: Eardley Ian 
Published: February 2020

Abstract
Male sexual dysfunction is common, with the most common types being erectile dysfunction, premature ejaculation, penile deformity, and priapism. Erectile dysfunction is common, becomes commoner with increasing age, and is often associated with cardiovascular disease and its risk factors. Patient assessment should seek to identify causative risk factors and treatment in the first instance is usually the management of risk factors and oral pharmacotherapy with a phosphodiesterase type 5 inhibitor. In women, sexual desire disorders are commoner in older postmenopausal women and a new treatment, flibanserin, has recently been licensed for this indication. Sexual arousal disorders in women also become more common postmenopausally and have a multifactorial aetiology. Treatment should be directed at the aetiological factor in the first instance while trials of oral pharmacotherapy for this condition have been disappointing.
Diabetes
Authors: Dayan Colin , Platts Julia 
Published: February 2020

Abstract
Diabetes mellitus can be defined as a state of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues, notably the retina, kidney, nerves, and arteries. It is due to inadequate production of insulin and/or ‘resistance’ to the glucose lowering and other actions of insulin, and is a significant and growing threat to global health, affecting more than 400 million people worldwide. Diabetes is a significant and growing threat to global health. Worldwide, diabetes affects more than 400 million people. This number was more than 10-fold less in 1985 (30 million) and the world prevalence is predicted to reach 640 million by 2040, with 10% of all adults affected.
The pineal gland and melatonin
Authors: Arendt J. , Cox Timothy M. 
Published: February 2020

Abstract
The pineal gland transduces light–dark cycles for the timing of body rhythms by secretion of melatonin, an endogenous indoleamine derived from tryptophan, the concentrations of which in plasma and cerebrospinal fluid are up to 100 times higher at night than in the daytime. This exerts its effects through transmembrane, G-protein coupled receptors (MT1 and MT2), and nuclear receptors primarily in the suprachiasmatic nucleus, pars tuberalis of the pituitary gland and hypothalamus. The natural period of the human circadian system is on average 24.1 to 24.3 h, and the principal resetting agent is light. Exogenous melatonin can shift the timing of the internal clock to earlier and later times, and synchronize a free-running clock that is not properly entrained to the 24-h day, hence it may have a therapeutic role for disorders of sleep rhythm including jet lag, in shift workers, and in blind people.
Nutrition in pregnancy
Authors: Williams David J. 
Published: February 2020

Abstract
Nutritional requirements for healthy pregnancy vary according to a woman’s pre-pregnancy nutritional state and her access to food during pregnancy: there is no unifying nutritional advice that is appropriate for all pregnant women throughout the world, or even within nations. Around the world, obesity and excessive gestational weight gain are now more common risk factors for pregnancy complications than undernutrition. Compared with mothers who have a normal body mass index or BMI (18.5–24.9 kg/m2), obese mothers have an increased risk of gestational diabetes, pre-eclampsia, caesarean delivery, stillbirth, congenital malformations, and large for gestational age babies. Underweight mothers have an increased risk of small for gestational age babies, and preterm birth. Paternal obesity has a negative effect on fetal growth, probably mediated by inheritance of insulin resistance. Both low birth weight and high birth weight babies have an increased risk of obesity in later life.
Diabetes in pregnancy
Authors: Jones Bryony , Dornhorst Anne 
Published: February 2020

Abstract
Diabetes in pregnancy is predominantly either pre-existing type 1 or type 2 diabetes mellitus, or gestational diabetes, the latter defined as diabetes or glucose intolerance first diagnosed during the pregnancy. Gestational diabetes usually arises in the late second trimester and is common, affecting from 2–6% to 15–20% of pregnant women depending on diagnostic criteria and country of origin. Gestational diabetes is most commonly diagnosed on the basis of an oral glucose tolerance test performed at 24–28 weeks’ gestation by a plasma glucose at 0 minutes of more than 5.1 (or &gt;5.6, depending on the authority) mmol/L, or at 120 minutes of more than 8.5 (or &gt;7.8) mmol/L. The effect of pregnancy on maternal glycaemic control ceases very quickly post-partum, hence women with pre-existing diabetes taking insulin should immediately revert to their pre-pregnancy regimen after birth, but with a lower insulin dose.
Neurological conditions in pregnancy
Authors: Dassan Pooja 
Published: February 2020

Abstract
Pregnancy can influence the clinical course of an underlying neurological problem or precipitate the first presentation of a neurological disease. This chapter looks at the various ways pregnancy can affect those suffering from epilepsy, multiple sclerosis, or cerebrovascular disease. In epilepsy, sodium valproate is associated with higher risk of major congenital malformations and impaired neuropsychological development than other antiepileptic drugs: lamotrigine or levetiracetam are preferred. Women taking antiepileptic drugs can breastfeed. In multiple sclerosis, the relapse rate is reduced in pregnancy, but substantially increased for three months post-partum. For cerebrovascular disease, stroke syndromes specific to pregnancy include pre-eclampsia, which can lead to posterior reversible vasoconstriction syndrome. Reversible cerebral vasoconstriction syndrome presents after delivery and has many similarities to posterior reversible vasoconstriction syndrome. There are conflicting opinions as to whether pregnancy or delivery increases the risk of cerebral aneurysm or arteriovenous malformation rupture.
Maternal infection in pregnancy
Authors: Burton Rosie 
Published: February 2020

Abstract
This chapter will consider infection with human immunodeficiency virus (HIV), tuberculosis, and malaria in pregnancy. The global roll-out of antiretroviral therapy has significantly improved survival for people living with HIV and reduced mother-to-child transmission, but HIV infection remains a leading cause of maternal mortality, infant death, and early childhood death. Most women with HIV infection are in sub-Saharan Africa, where the highest prevalence is among young women of reproductive age. Meanwhile, tuberculosis is a major cause of maternal mortality. Active tuberculosis also adversely affects pregnancy outcomes, with an increased risk of preterm delivery, growth restriction, and perinatal death. Malaria is a major cause of maternal and neonatal morbidity and mortality. Pregnant women are more susceptible to malaria, have more severe disease, and may deteriorate rapidly. In severe malaria, mortality is 15–20% in non-pregnant women, compared to 50% in pregnancy. Primigravidae are at highest risk of severe malaria and death.
Blood disorders in pregnancy
Authors: Perry David J. , Lowndes Katharine 
Published: February 2020

Abstract
Plasma volume increases by more during pregnancy than does red cell mass, leading to haemodilution and a fall in the haematocrit from about 40% to 33%, with a nadir usually reached at 24–32 weeks’ gestation. Anaemia during pregnancy is defined as a haemoglobin concentration of below 105 g/L during the second and third trimesters and below 110 g/L in the first trimester. The commonest haematological problem encountered in pregnancy is iron-deficiency anaemia. Routine iron supplementation in all pregnant women is probably not justified in developed countries, but if iron deficiency is detected it is advisable to treat as early as possible. Normal pregnancy is associated with marked changes in all aspects of haemostasis, the overall effect of which is to generate a state of hypercoagulability. These changes in haemostasis, while reducing the risks of excessive blood loss at delivery, significantly increase the risk of venous thromboembolic disease in pregnancy.
Immune disorders of the gastrointestinal tract
Authors: Bhattacharyya Joya , Kaser Arthur 
Published: February 2020

Abstract
Immune homeostasis in the gut is the result of a delicate balance between peaceful coexistence with commensal microbiota, immunomodulatory effects of dietary antigens, and appropriate responses to pathogens. Immune disorders of the gut arise when defects in the integrity of these components lead to a dysregulated immune response to the commensal environment. Primary immunodeficiency syndromes can present with intestinal inflammation but are commonly characterized by an increased susceptibility to infections in childhood. Secondary immunodeficiency can occur in a protein-losing enteropathy where loss of immunoglobulins and lymphocytes increase susceptibility to infections, or as a result of metabolic diseases (e.g. diabetes or liver cirrhosis), infections (e.g. HIV), or drugs (e.g. chemotherapy). Immunosuppressive medication can not only lead to secondary immunodeficiency but in the context of neutropenia, cytotoxic gastrointestinal mucosal injury can lead to neutropenic typhlitis. Graft-versus-host disease arises from host antigen-presenting cells engaging with donor T cells and triggering an inflammatory cascade. Immunotherapy with checkpoint inhibitors can have significant gastrointestinal immune-related adverse effects, most notably enterocolitis. Autoimmune diseases can impact gastrointestinal function. Autoimmune dysautonomia can result in gastrointestinal-specific dysmotility and systemic IgG4-related disease can lead to autoimmune pancreatitis. Systemic autoimmune diseases can have gastrointestinal manifestations related to the primary autoimmune process or as an adverse effect of treatment. Hypersensitivity reactions to dietary antigens (e.g. peanuts) result in food allergies and can be either IgE or non-IgE mediated. Food intolerance which is not immunologically mediated is the result of pharmacological (e.g. monosodium glutamate), enzyme-related (e.g. lactose intolerance), or noncoeliac gluten sensitivity. Eosinophilic gastrointestinal tract disorders are often associated with a food allergen: treatment is with steroids and avoidance of the allergen.
Hormones and the gastrointestinal tract
Authors: Scott Rebecca , Tan T.M. , Bloom S.R. 
Published: February 2020

Abstract
The gastrointestinal tract is the largest endocrine organ in the body, with its component cells dispersed along its length rather than being clustered in glands. More than 20 gut peptides integrate gastrointestinal function by regulating the actions of the epithelium, muscles, and nerves; they also affect the growth and development of the gut and have a major role in appetite control. They mostly work in an autocrine or paracrine manner.
Gastrointestinal hormones include the gastrin–cholecystokinin family, the secretin superfamily, preproglucagon derivatives, the motilin–ghrelin family, the pancreatic polypeptide-fold family, and various other gut peptides. Gastrointestinal and other diseases may cause abnormalities of these gut peptides, for example: (1) achlorhydria (from atrophic gastritis or drug-induced) causes elevation of circulating gastrin; (2) malabsorptive conditions are associated with a decrease in the amount of peptides produced in the affected region, and a compensatory elevation of other peptides; and (3) obesity is associated with orexigenic (appetite-stimulating) and less satiating hormonal changes, and the beneficial effects of bariatric surgery are partly explained through alterations in gut hormones.