Książki: „Airway inflammation”

1

Rogers, Duncan F., i Louise E. Donnelly. Human Airway Inflammation. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591515.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

2

Tony, Eissa N., i Huston David P, red. Therapeutic targets in airway inflammation. New York: Marcel Dekker, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

3

1940-, Olivieri D., i Bianco S, red. Airway obstruction and inflammation: Present status and perspectives. Basel: Karger, 1990.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

4

Underwood, Stephen L. Studies on the mechanisms of pulmonary inflammation and airway hyperreactivity in animal models of asthma. London: University of East London, 1997.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

5

Page, Clive P., Katharine H. Banner i Domenico Spina, red. Cellular Mechanisms in Airways Inflammation. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

6

Eissa, N. Tony, i David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

7

Eissa, N. Tony, i David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

8

Eissa, N. Tony, i David P. Huston, red. Therapeutic Targets in Airway Inflammation. CRC Press, 2003. http://dx.doi.org/10.3109/9780203911471.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

9

Eissa, N. Tony, i David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

10

Eissa, N. Tony, i David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

11

Eissa, N. Tony, i David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

12

(Editor), Clive P. Page, Katharine H. Banner (Editor) i Domenico Spina (Editor), red. Cellular Mechanisms in Airways Inflammation (Progress in Inflammation Research). Birkhauser, 2000.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

13

1947-, Nijkamp Franciscus Petrus, red. Mediators in airway hyperreactivity. Basel: Birkhäuser Verlag, 1990.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

14

Rogers, Duncan F., i Louise E. Donnelly. Human Airway Inflammation: Sampling Techniques and Analytical Protocols. Humana Press, 2013.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

15

(Editor), C. P. Page, Katharine H. Banner (Editor) i Domenico Spina (Editor), red. Cellular Mechanisms in Airways Inflammation (Pir (Series).). Birkhauser, 2000.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

16

Obstructive Airway Diseases. Taylor & Francis Group, 2011.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

17

Roldán, Nestor González, Otto Holst, Johannes Huebner i Katarzyna Anna Duda, red. Role of Lipids in the Dynamics of Allergic Airway Inflammation. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-315-6.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

18

Olivieri, D. Airway Obstruction and Inflammation: Present Status and Perspectives (Progress in Respiratory Research). S. Karger AG (Switzerland), 1989.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

19

(Editor), Duncan F. Rogers, i Louise E. Donnelly (Editor), red. Human Airway Inflammation: Sampling Techniques and Analytical Protocols (Methods in Molecular Medicine). Humana Press, 2001.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

20

Fahy, John Vincent. Cellular and biochemical analysis of induced sputum: A novel method for studying airway inflammation and mucus hypersecretion in asthmatic subjects. Wyd. 2. 1995.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

21

Ray, Abhijit, i Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2016.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

22

Ray, Abhijit. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2011.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

23

Ray, Abhijit, i Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2016.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

24

Ray, Abhijit, i Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2018.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

25

(Editor), Johan Zaagsma, Herman Meurs (Editor) i Ad F. Roffel (Editor), red. Muscarinic Receptors in Airways Diseases (Progress in Inflammation Research). Birkhauser, 2001.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

26

Jeffrey, Andrew, Abdul Nasimudeen i Joshua Agbetile. Asthma. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0133.

Pełny tekst źródła

Streszczenie:

Asthma is a disorder of airway smooth muscle and airway inflammation, manifested by variable airflow limitation. This definition continues to be refined in light of developments in the understanding of asthma’s pathophysiology, immunology, and treatment.

Style APA, Harvard, Vancouver, ISO itp.

27

Williams, Erin S. Asthmatic for Adenotonsillectomy. Redaktorzy Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel i Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0005.

Pełny tekst źródła

Streszczenie:

Asthma is a chronic reversible pulmonary condition. It is the most common respiratory disease as it affects 6 million to 9 million children in the United States. The patient with asthma can experience reversible bronchoconstriction, airway inflammation, airway hyperresponsivness, and increased mucus production. Inflammation is the fundamental abnormality. This dynamic process exists on a spectrum of mild, moderate, or severe. Patients may exhibit expiratory wheezing, obstruction to expiration, and/or inspiration, cough, and respiratory distress. Given the prevalence of asthma and its potential for significant morbidity and mortality, it is important that the anesthesiologist be able to determine the severity of disease and prevent and/or treat bronchospasm.

Style APA, Harvard, Vancouver, ISO itp.

28

Redding, Amanda T., i Marc Hassid. Acute Severe Asthma and Bronchospasm. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0079.

Pełny tekst źródła

Streszczenie:

This chapter focuses on acute asthma and bronchospasm occurring in the perioperative period. Over 6% of the people in the United States have asthma, which is characterized by chronic inflammation, airway hyperresponsiveness, excessive mucus, and reversible airway obstruction. Due to generalized airway hyperreactivity, a history of asthma increases the risk of coughing, wheezing, bronchospasm, and oxygen desaturation. Although the incidence of bronchospasm associated with asthma is low, when it occurs it is often severe. A stepwise treatment algorithm is defined, which covers the use of first line agents such as inhaled beta-2 agonists and steroids, but also agents that are useful for refractory cases such as epinephrine, magnesium, and possibly ketamine.

Style APA, Harvard, Vancouver, ISO itp.

29

Hebestreit, Helge, Susi Kriemler i Thomas Radtke. Exercise, physical activity, and asthma. Redaktorzy Neil Armstrong i Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0024.

Pełny tekst źródła

Streszczenie:

The incidence of asthma in children varies among countries and can be estimated to range between 5% and 20%. Exercise-induced asthma (EIA) is common in patients with asthma but can also occur in some children without asthma. Typical symptoms of EIA include cough, chest tightness, and shortness of breath shortly after exercise. The pathophysiology of EIA is not completely understood, but it has been shown that airway cooling and drying with increased ventilation during exercise and airway re-warming after exercise play a pivotal role. In addition, a lack of physical activity may also contribute to EIA. Regular exercise may increase fitness and psychological well-being but may also positively influence airway inflammation in children with asthma. The diagnosis of EIA is based on the typical history and may be verified by an exercise challenge test. Every child with EIA should be able to engage in all type of physical activities.

Style APA, Harvard, Vancouver, ISO itp.

30

Page, C. P. Cellular Mechanisms in Airways Inflammation. Springer, 2012.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

31

M, Geddes Duncan, Kay A. B i Friend J. A. R, red. Inflammation: Its significance in airways disease. London: Medical Tribune Group, 1987.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

32

Rello, Jordi, i Bárbara Borgatta. Pathophysiology of pneumonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0115.

Pełny tekst źródła

Streszczenie:

Airway colonization, ventilator-associated tracheobronchitis (VAT), and hospital-acquired (HAP) and ventilator-associated pneumonia (VAP) are three manifestations having the presence of micro-organisms in airways in common. Newer definitions have to consider worsening of oxygenation, in addition to purulent respiratory secretions, chest-X rays opacities, and biomarkers of inflammation. Bacteria are the main causes of HAP/VAP. During hospitalization there’s a shift of airway’s colonizing flora from core organisms to enteric and non-fermentative ones. Macro- and micro-aspiration is the most important source of pneumonia. Endotracheal tube secretion leakage is an important source, serving biofilm as a reservoir. Exogenous colonization is infrequent, but it may contribute to cross-infection with resistant species. Prevention of VAP can be achieved by implementing multidisciplinary care bundles focusing on oral/hand hygiene and control of sedation. Pneumonia develops when micro-organisms overwhelm host defences, resulting in a multifocal process. Risk and severity of pneumonia is determined by bacterial burden, organism virulence and host defences. Innate and adaptive immune responses are altered, decreasing clearing of pathogens. Some deficits of the complement pathway in intubated patients are associated with increased risk for VAP and higher mortality. Micro-arrays have demonstrated specific different immunological signatures for VAP and VAT. Early antibiotic therapy is associated with a decrease in early HAP/VAP incidence, but selects for MDR organisms. Attributable mortality is lower than 10%, but HAP/VAP prolongs length of stay, and dramatically increase costs and use of health care resources.

Style APA, Harvard, Vancouver, ISO itp.

33

Balhara, Kamna S., Basem F. Khishfe i Jamil D. Bayram. Sepsis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0004.

Pełny tekst źródła

Streszczenie:

Sepsis is a clinical syndrome characterized by systemic inflammation in the presence of infection. The source of infection may be occult. One must be aware of the epidemiology, presenting features and complications, diagnostic considerations and tests, and the organisms involved. Bacteria (gram positive and negative) are most commonly associated with sepsis, although fungi, viruses, and parasites can cause sepsis. Infections in the lungs, urinary tract, abdomen, skin, brain, and other areas can cause bacteremia and lead to sepsis. Treatment includes airway, breathing, and circulation (ABCs) management; aggressive fluid resuscitation; early administration of broad-spectrum antibiotics; and early goal-directed therapy and severe sepsis resuscitation bundle. Diagnosis can be challenging in pediatric and geriatric populations.

Style APA, Harvard, Vancouver, ISO itp.

34

Wecksell, Matthew, i Kenneth Fomberstein. Traumatic Brain Injury and C-Spine Management. Redaktorzy David E. Traul i Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0020.

Pełny tekst źródła

Streszczenie:

Traumatic brain injury encompasses two different types of pathology: that caused at the time of the initial physical insult, called primary injury, and then further, secondary injury caused by either host cellular responses such as oxidative injury and inflammation or by physiological insults such as ischemia, hypoxia, hypo- or hypercapnia, intracranial hypertension, and hypo- or hyperglycemia. While primary injury falls to the realm of public health (e.g., encouraging helmet use for sports, discouraging impaired driving, etc.), many secondary injuries are avoidable with proper medical management. As the stem case for this chapter, an older patient experiences a fall and is incoherent on presentation to the emergency room. This case concerns her initial management, stabilization, diagnosis, and airway management. With progression of her traumatic brain injury, the authors discuss intracranial pressure management, surgical management, and resuscitation as well as likely postoperative sequelae.

Style APA, Harvard, Vancouver, ISO itp.

35

Kriemler, Susi, Thomas Radtke i Helge Hebestreit. Exercise, physical activity, and cystic fibrosis. Redaktorzy Neil Armstrong i Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0027.

Pełny tekst źródła

Streszczenie:

Cystic fibrosis (CF) is a genetic disease resulting in an impaired mucociliary clearance, chronic bacterial airway infection, and inflammation. The progressive destruction of the lungs is the main cause of morbidity and premature death. Diverse other organ systems such as heart, muscles, bones, gastro-intestinal tract, and sweat glands are often also affected and interfere with exercise capacity. Hence, exercise capacity is reduced as the disease progresses mainly due to reduced functioning of the muscles, heart, and/or lungs. Although there is still growing evidence of positive effects of exercise training in CF on exercise capacity, decline of pulmonary function, and health-related quality of life, the observed effects are encouraging and exercise should be implemented in all patient care. More research is needed to understand pathophysiological mechanisms of exercise limitations and to find optimal exercise modalities to slow down disease progression, predict long-term adherence, and improve health-related quality of life.

Style APA, Harvard, Vancouver, ISO itp.

36

Gilchrist, Francis J., i Alex Horsley. Management of respiratory exacerbations. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0005.

Pełny tekst źródła

Streszczenie:

Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also be optimized. Mild exacerbations are usually treated with oral antibiotics and more severe exacerbations with intravenous antibiotics. The choice of antibiotic is guided by the patient’s chronic pulmonary infections, the in-vitro antibiotic sensitivities, known antibiotic allergies, and the previous response to treatment. In patients with chronic Pseudomonas aeruginosa infection, antibiotic monotherapy is thought to increase the risk of resistance and treatment with 2 antibiotics is therefore suggested (usually a β‎-lactam and an aminoglycoside). Although there is a lack of evidence on the duration of treatment, most patients receive around 14 days. This can be altered according to the time taken for symptoms and lung function to return to pre-exacerbation levels. If patients are carefully selected and receive appropriate monitoring, home intravenous antibiotics can be as effective as in-patient treatment. They are also associated with decreased disruption to patients / family life, decreased risk of cross infection and decreased costs.

Style APA, Harvard, Vancouver, ISO itp.

37

Frew, Anthony. Air pollution. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

Pełny tekst źródła

Streszczenie:

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

Style APA, Harvard, Vancouver, ISO itp.

38

Raeburn, D. Ed. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators & Signal Transduction (Exs). Birkhauser, 1996.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

39

1953, Raeburn D., i Giembycz M. A. 1961-, red. Airways smooth muscle: Neurotransmitters, amines, lipid mediators, and signal transduction. Basel: Birkhauser Verlag, 1995.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

40

Davey, Patrick, Sherif Gonem i David Sprigings. Interstitial lung disease. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0139.

Pełny tekst źródła

Streszczenie:

The interstitial lung diseases, also known as the diffuse or diffuse parenchymal lung diseases, are a broad group of pulmonary disorders which mainly affect the lung parenchyma as opposed to the airways. By convention, infectious and malignant conditions are excluded from this definition. Thus, the interstitial lung diseases comprise a group of conditions characterized by variable degrees of inflammation and fibrosis, centred on the lung interstitium and alveolar airspaces.

Style APA, Harvard, Vancouver, ISO itp.

41

Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction (Respiratory Pharmacology and Pharmacotherapy). Birkhauser Boston, 1995.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

42

Inflammation,its significance in airways disease: Proceedings of a series of symposia held in Edinburgh, London and Chester in October and November, 1986. London: Education in Practice, 1987.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

43

Amin, Kawa. The Relationship Between Inflammation and Structural Changes in the Airways of the Lower and Upper Respiratory Tract: Studies in Patients With Asthma, ... Summaries of Uppsala Dissertations, 932). Uppsala Universitet, 2000.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

44

Sahetya, Sarina. Acute Uncomplicated Bronchitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0029.

Pełny tekst źródła

Streszczenie:

Acute bronchitis is a respiratory illness characterized predominantly by cough with or without sputum production that lasts for up to 3 weeks in the presence of normal chest radiography. Additional presenting symptoms include rhinorrhea, congestion, sneeze, sore throat, wheezing, low-grade fever, myalgia, and fatigue. Causative organisms include viral and bacterial pathogens. The disease course is characterized by self-limited inflammation of the airways. Chest radiographs should be utilized to distinguish acute bronchitis from pneumonia or interstitial disease. Therapeutic recommendations are typically supportive; however, studies reveal that between 60% and 80% of patients receive unwarranted antibiotic therapy. Only those patients at high risk for serious complications (including patients over 65 with a history of hospitalization, diabetes mellitus, congestive heart failure, or current use of oral glucocorticoids) usually require routine antibiotic therapy directed toward both typical and atypical bacterial pathogens.

Style APA, Harvard, Vancouver, ISO itp.

Książki na temat „Airway inflammation”

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych