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ch 12 stoichiometry study guide answersThe current custom error settings for this application prevent the details of the application error from being viewed remotely (for security reasons). It could, however, be viewed by browsers running on the local server machine. Physics Chemistry Statistics Economics Accounting Computer Science Find solutions for your homework Search Search Search done loading home study Science Biology General Biology General Biology solutions manuals Biology Laboratory Manual 10th edition chapter 37 We have 94 solutions for your book. We have 94 solutions for your book. Problem 1Q Chapter Chapter List CH37 CH1 CH2 CH3 CH4 CH5 CH6 CH7 CH8 CH9 CH10 CH11 CH12 CH13 CH14 CH15 CH16 CH17 CH18 CH19 CH20 CH21 CH22 CH23 CH24 CH25 CH26 CH27 CH28 CH29 CH30 CH31 CH32 CH33 CH34 CH35 CH36 CH37 CH38 CH39 CH40 CH41 CH42 CH43 CH44 CH45 CH46 CH47 CH48 CH49 CH50 CH51 Problem Problem List 1Q 1Q 1QFT 2Q 2QFT 3Q 3QFT 4Q 4QFT 5Q 5QFT 6Q 7Q 8Q a. What features of Dugesia distinguish its head from its tail? b. What is the difference between the eyes of most animals you are familiar with and the eyespots of Dugesia ? c. How does the head of Dugesia move differently from the tail? d. Does Dugesia move randomly or in an apparent direction? e. How is Dugesia adapted for directional movement? f. How does a flatworm respond when touched with a probe? g. Do the planaria move toward or away from light? h. Where is the feeding tube located. Why is this unusual for bilaterally symmetrical organisms? i. Is the gastrovascular cavity of Dugesia a simple sac. How is it divided and what advantage do these divisions offer? j. Consider objective 1 listed at the beginning of this exercise. How could being monoecious contribute to evolutionary success of flatworms in their environment? k. Planarians have a head. In biological terms, what constitutes a “head”. How does it relate to objectives 1, 4, and 7? l. Planaria lack specialized gas-exchange organs. How do you think planaria accomplish this task.http://www.mohini.cn/fckeditor/editor/filemanager/connectors/php/fckeditor/upload/202010/epson-7900-service-manual-download.xml

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Step-by-step solution This problem hasn’t been solved yet. View the primary ISBN for: Biology Laboratory Manual 10th Edition Textbook Solutions This is an alternate ISBN. All rights reserved. The experiments and procedures are simple, safe, easy to perform, and especially appropriate for large classes. Few experiments require more than one class meeting to complete the procedure. Each exercise includes many photographs, traditional topics, and experiments that help students learn about life. Procedures within each exercise are numerous and discrete so that an exercise can be tailored to the needs of the students, the style of the instructor, and the facilities available.Click continue to view and update your selected titles.See tabs below to explore options and pricing. Don't forget, we accept financial aid and scholarship funds in the form of credit or debit cards. Check with your instructor to see if Connect is used in your course. Pricing subject to change at any time.Randy was awarded the 1993 Teacher Exemplar Award by the National Association of Biology Teachers (NABT). Other awards and honors include a Fulbright Scholarship, a listing in the Who's Who in Science and Engineering, 1986 Most Outstanding Teacher from Baylor University, and 1980 Most Outstanding Teaching Assistant from UCLA. He received his Ph.D. in Plant Development from UCLA Virtually every exercise of this manual is now accompanied by tailor-made multimedia resources. You can access a variety of high-definition videos, PowerPoint presentations, and other resources that demonstrate basic techniques, emphasize biological principles, test for understanding, and engage students as they learn biology in the laboratory. Quickly access registration, attendance, assignments, grades, and course resources in real time in one, familiar location. We have put in place processes to make accessibility and meeting the WCAG AA guidelines part of our day-to-day development efforts and product roadmaps.http://www.mahalaxmiornament.com.np/userfiles/epson-7900-printer-manual.xmlThese links are provided as supplementary materials, and for learners’ information and convenience only. McGraw-Hill has no control over and is not responsible for the content or accessibility of any linked website.Randy was awarded the 1993 Teacher Exemplar Award by the National Association of Biology Teachers (NABT). McGraw-Hill has no control over and is not responsible for the content or accessibility of any linked website.By continuing to browse this site you are agreeing to our use of cookies. Find out more here. This amount of air provides enough oxygen for the body when the person is resting. It is possible to inhale more deeply and exhale more forcefully than usual. The maximum amount of air moved in and out of the lungs when the deepest possible inspiration is followed by the strongest possible expiration is called the vital capacity. In this investigation, you will determine the tidal volume and vital capacity of your lungs. Problem How are the tidal volume and vital capacity of the human lungs measured. Pre- Lab Discussion Read the entire investigation. Then, work with a partner to answer the following questions. 1. Why is it important to measure tidal volume and tidal capacity more than once and then calculate means for these measurements. Calculating the mean for several trials should help to compensate for small measurement errors and other sources of uncertainty. 2. What would you conclude if the balloon were smaller during your vital capacity measurement than during your tidal volume measurement. This result would suggest an error in conducting the experiment. Sources of error could include using balloons of different original sizes or of different elastic strengths, over-inhaling or -exhaling during the tidal volume measurement, under-inhaling or -exhaling during the vital capacity measurement, errors of mathematics or of interpreting graphs, and so on. 4. How do you expect your estimated vital capacity to compare to your measured vital capacity. Explain your answer. Student predictions may reflect their knowledge of the effects of aerobic training on vital capacity and whether or not they perceive themselves as well-trained.Thank you, for helping us keep this platform clean. The editors will have a look at it as soon as possible. Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Show details Walker HK, Hall WD, Hurst JW, editors. Boston: Butterworths; 1990.Definition A wheeze is a high-pitched, musical, adventitious lung sound produced by airflow through an abnormally narrowed or compressed airway(s). A wheeze is synonymous with a high-pitched or sibilant rhonchus. Asthma is a heterogeneous syndrome characterized by variable, reversible airway obstruction and abnormally increased responsiveness (hyperreactivity) of the airways to various stimuli. The resulting airflow obstruction may be chronic or episodic, with respiratory symptoms resolving either spontaneously or as a result of therapy (bronchodilators or corticosteroids). A generally accepted definition of asthma does not yet exist because the syndrome has different causes, mechanisms, clinical features, and responses to therapy. Technique Wheezing is a subjective complaint that may be described in various ways. Some patients report noisy, difficult breathing (wheezy dyspnea), whereas others describe a whistling type of breathing or rattling secretions in the throat. The majority of asthmatic patients who report active wheezing generally have this finding documented by the examining physician. Nevertheless, wheezing is not always present during active asthma, and its absence should not exclude the diagnosis. Some patients with chronic asthma may become accustomed to wheezing and do not volunteer this information unless specifically asked. Most patients with asthma complain more frequently about chest tightness (in combination with shortness of breath or cough) than wheezing. Thus, any patient with chronic or episodic respiratory symptoms or who presents with a history of asthma or other chronic airway disease should be asked about wheezing. The diagnosis of asthma is usually obvious from the patient's history. It should be highly suspected from a description of episodic and variable respiratory symptoms (with or without wheezing) or recurrent chest colds and bronchitis (productive cough). A careful, thorough history is fundamental not only in arriving at an accurate diagnosis but also in determining the severity of an individual's asthma and its appropriate therapy. The clinician should inquire about the following: General (relating to the overall course of asthma in an individual): Specific (relating to acute episode in an individual): The airway narrowing may be caused by bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor, foreign body, or tenacious secretions. Wheezes are believed to be generated by oscillations or vibrations of nearly closed airway walls. Air passing through a narrowed portion of an airway at high velocity produces decreased gas pressure and flow in the constricted region (according to Bernoulli's principle). The internal airway pressure ultimately begins to increase and barely reopens the airway lumen. The flow rate and mechanical properties of the adjacent tissues that are set into oscillation determine the intensity, pitch, composition (monophonic or polyphonic notes), duration (long or short), and timing (inspiratory or expiratory, early or late) of this dynamic symptom and sign. Wheezes are heard more commonly during expiration because the airways normally narrow during this phase of respiration. Wheezing during expiration alone is generally indicative of milder obstruction than if present during both inspiration and expiration, which suggests more severe airway narrowing. However, most asthmatic patients are unable accurately to correlate their wheezing (or other respiratory symptoms) to the severity of airway obstruction as measured objectively by pulmonary function tests. In contrast, the absence of wheezing in an asthmatic may indicate either improvement of the bronchoconstriction or severe, widespread airflow obstruction. The latter suggests that the airflow rates are too low to generate wheezes or the viscous mucus is obstructing large regions of the peripheral airways. In asthma, the markedly increased airway resistance (airflow obstruction) contributes to the characteristic physiologic and clinical changes observed during active or symptomatic periods. Airways tend to close early during expiration, and hyperinflation results. Although breathing at high lung volumes tends to maintain open airways, this response demands increased muscular work of breathing to provide adequate ventilation, which is increased secondary to stimulation of airway receptors and hypoxia. Most asthmatics complain of greater difficulty during inspiration than expiration, due to the uncomfortable work of breathing necessary to ventilate hyperinflated, abnormally stiff, or noncompliant lungs. Several hypotheses have been proposed to explain the pathogenesis of bronchoconstriction and other airway abnormalities in asthma. None completely accounts for all the clinical forms of asthma. The proposed mechanisms probably overlap and interrelate even in the same individual. This immunologic reaction results in the release of potent biochemical mediators that contract bronchial smooth muscle, increase vascular permeability and mucus secretion, and attract inflammatory cells. Preformed histamine, neutrophil and eosinophil chemotactic factors, and platelet-activating factors are released. Type III (arthus) immunologic reactions have also been implicated in some cases of asthma and in the related allergic bronchopulmonary aspergillosis. This nonimmunologic hypothesis stresses the importance of the parasympathetic nervous system (vagus nerve) in regulating airway caliber. Chemical or mechanical inflammation stimulates cholinergic irritant receptors in the airway mucosa to hyperreact, leading to vagally mediated reflex bronchoconstriction. This reflex is produced by either direct mediator release or secondary stimulation of irritant receptors by smooth muscle constriction. Beta-adrenergic stimulation increases cyclic 3,5-adenosine monophosphate (AMP) and decreases cyclic 3,5-guanosine monophosphate (GMP), resulting in smooth muscle relaxation (bronchodilation). Beta-adrenergic inhibition produces opposite effects, resulting in bronchoconstriction. Therefore, asthmatics may have relative beta-adrenergic hyporesponsiveness and an imbalance between adrenergic and cholinergic regulation that favor the latter, resulting in greater than normal mediator generation and unopposed bronchoconstriction. The differential diagnosis of wheezing is long ( Table 37.2 ) and, at times, complicated, particularly if asthma coexists with another pulmonary disease. Table 37.2 Differential Diagnosis of Wheezing. Wheezing may be acute or chronic (recurrent) in children with nonasthmatic disorders. Acute wheezing in small children suggests bronchiolitis, particularly if the child was well prior to an upper respiratory tract infection (frequently respiratory syncytial virus) and has relatively irreversible airway obstruction without evidence of atopy. Many children with acute bronchiolitis may develop asthma; the long-term course of the illness may be the best diagnostic determinant because bronchiolitis does not usually recur. In a child, wheezing that is most prominent during inspiration suggests laryngotracheobronchitis (croup), epiglottitis, aspiration of a foreign body, or congenital laryngeal or tracheal narrowing. Wheezing occurs during both inspiration and expiration as the airway caliber becomes increasingly smaller. Chronic wheezing and respiratory infections in a child should raise the possibility of cystic fibrosis, with or without gastrointestinal complaints. Adults with a new onset of wheezing generally have different nonasthmatic disorders from those in children. In adults, stridor or localized wheezing may be caused by mechanical obstruction of a central airway, such as by a tumor, foreign body (especially food), goiter, or stenosis. In addition to laryngeal edema (resulting from angioedema or anaphylaxis) and vocal cord paralysis, some individuals may have spastic adduction of the vocal cords due to functional or psychological factors. Transient wheezing occurs in some patients with pulmonary embolism, the carcinoid syndrome, and systemic mastocytosis as a result of the release of bronchoactive amines or mediators. Parenchymal lung disorders such as sarcoidosis, extrinsic allergic alveolitis, and the adult respiratory distress syndrome (non-cardiogenic pulmonary edema) can occasionally produce wheezing due to airway compromise by granulomas or edema fluid, release of mediators, or underlying asthma. A large group of diseases characterized by pulmonary infiltrates and peripheral blood eosinophilia may produce asthma-like wheezing: Loeffler's syndrome, chronic eosinophilic pneumonia, tropical eosinophilia, hypereosinophilic syndrome, various vasculitides, and allergic bronchopulmonary aspergillosis. A specific, often seasonal antigen characteristically produces a type I hypersensitivity reaction, resulting in paroxysmal bronchoconstriction. Eosinophils in the sputum, eosinophilia, increased IgE, and positive skin tests for immediate hypersensitivity are common findings. Intrinsic (nonallergic or infective) asthma occurs primarily in adulthood (more than 30 years of age) and is not usually associated with atopy, seasons, eosinophilia, increased IgE, or positive skin tests. These patients are hyperreactive to a wide variety of stimuli and have some intrinsic abnormality of bronchomotor tone. In many patients the onset of asthma is preceded by an upper respiratory infection, and asthmatic symptoms tend to persist for years with variations in severity rather than asymptomatic remissions. Asthmatic bronchitis occurs in elderly, nonatopic patients who have a long or heavy smoking history and active chronic cough and sputum production with superimposed hyperreactive airways. The latter is supported by partial reversal of airway obstruction by bronchoconstriction during inhalation challenge with methacholine or histamine. Sinusitus and sputum rich in polymorphonuclear leukocytes (rather than eosinophils) are frequently present. Allergy evaluation is negative. Exercise-induced asthma occurs in the majority of asthmatic patients who exercise (e.g., running, cycling). Wheezing and dyspnea characteristically develop shortly after completion of a sustained physical activity and may be the only symptoms of asthma. The severity of the symptoms depends on the duration and type of exercise and how recently the individual previously exercised. This phenomenon is caused by respiratory heat or water loss, which then releases mast cell mediators. Drug-induced asthma occurs in patients shortly after exposure to certain medications (e.g., propranolol, timolol, aspirin, nonsteroidal anti-inflammatory agents, cholinergic drugs), additives (e.g., tartrazine, metabisulfite, alcohol), or certain medical procedures (e.g., studies using iodinated radiographic contrast dyes, hemodialysis). A patient with wheezing temporally related to aspirin ingestion, rhinitis, and nasal polyps suggests aspirin hypersensitivity. Foods may also contain potentially asthmagenic chemicals, such as monosodium glutamate and bisulfite preservative. In general, asthma related to these agents does not appear to have an immunologic mechanism and is more frequent in adult, nonatopic asthmatic patients. Occupational asthma may be provoked in susceptible individuals following exposure to irritants present in a work setting or at home. The list of occupations and related asthmagenic substances used or generated is long and continually expanding. A further discussion is presented in Chapter 41, Environmental Inhalation. Variant or atypical asthma occurs in some patients who present without wheezing but with acute or chronic cough or dyspnea as the sole symptom of asthma. Paroxysms of cough or dyspnea may or may not be related to a specific stimulus, season, time of day, activity, postnasal drip, or respiratory infection. Asthmatic patients with cough as the major or only symptom develop bronchoconstriction localized primarily in the central or large airways where subepithelial cough receptors abound and reflex bronchoconstriction occurs following exposure to various stimuli. Patients complaining of episodic dyspnea have involvement predominantly in the peripheral airways where bronchoconstriction, mucosal edema, and secretion contribute to the airway obstruction. Although most patients with atypical asthma are adults, the physical examination and routine pulmonary functions tests are not helpful (usually normal), making the diagnosis difficult and confusing. The diagnosis must begin with a high index of suspicion. This subgroup of asthmatics emphasizes the fact that wheezing is not always a cardinal manifestation of asthma. References. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. The clinical assessment of severe asthma. Lawlor GJ Jr, Tashkin DP. Asthma. In: Lawlor GJ Jr, Fischer TJ, eds. Manual of allergy and immunology: diagnosis and therapy. McFadden ER Jr,, Ingram RH Jr. Exercise-induced airway obstruction. Relationship of wheezing to the severity of obstruction in asthma. Statement by the Committee on Diagnostic Standards for Nontuberculous Respiratory Disease. Chronic bronchitis, asthma, and pulmonary emphysema. Asthma and anti-inflammatory drugs. Bronchial asthma. Mechanisms and therapeutics, 2d ed. Boston: Little, Brown, 1985. Williams MH, Jr, Shim CS. Asthma. In: Simmons DH, ed. Current pulmonology.Wheezing and Asthma. In: Walker HK, Hall WD, Hurst JW, editors. Hollingsworth HM. Clin Chest Med. 1987 Jun; 8(2):231-40. Seibert AF, Allison RC, Bryars CH, Kirkpatrick MB. Am Rev Respir Dis. 1989 Dec; 140(6):1805-6. See reviews. See all. Recent Activity Clear Turn Off Turn On Wheezing and Asthma - Clinical Methods Wheezing and Asthma - Clinical Methods Your browsing activity is empty. Activity recording is turned off. Turn recording back on See more. This website works best with modern browsers such as the latest versions of Chrome, Firefox, Safari, and Edge. If you continue with this browser, you may see unexpected results.If it doesn't, try opening this guide in a different browser and printing from there (sometimes Internet Explorer works better, sometimes Chrome, sometimes Firefox, etc.). Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License 4.0 license. Until that point, physicians did not understand that death sometimes followed blood transfusions, when the type of donor blood infused into the patient was incompatible with the patient’s own blood. Blood groups are determined by the presence or absence of specific marker molecules on the plasma membranes of erythrocytes. With their discovery, it became possible for the first time to match patient-donor blood types and prevent transfusion reactions and deaths. With RBCs in particular, you may see the antigens referred to as isoantigens or agglutinogens (surface antigens) and the antibodies referred to as isoantibodies or agglutinins. In this chapter, we will use the more common terms antigens and antibodies. Following an infusion of incompatible blood, erythrocytes with foreign antigens appear in the bloodstream and trigger an immune response. Proteins called antibodies (immunoglobulins), which are produced by certain B lymphocytes called plasma cells, attach to the antigens on the plasma membranes of the infused erythrocytes and cause them to adhere to one another. This process is called agglutination. This hemoglobin travels to the kidneys, which are responsible for filtration of the blood. However, the load of hemoglobin released can easily overwhelm the kidney’s capacity to clear it, and the patient can quickly develop kidney failure. People whose erythrocytes have A antigens on their erythrocyte membrane surfaces are designated blood type A, and those whose erythrocytes have B antigens are blood type B. People can also have both A and B antigens on their erythrocytes, in which case they are blood type AB. People with neither A nor B antigens are designated blood type O. ABO blood types are genetically determined. This is not the case for the ABO blood group. Individuals with type A blood—without any prior exposure to incompatible blood—have preformed antibodies to the B antigen circulating in their blood plasma. These antibodies, referred to as anti-B antibodies, will cause agglutination and hemolysis if they ever encounter erythrocytes with B antigens. Similarly, an individual with type B blood has pre-formed anti-A antibodies. Individuals with type AB blood, which has both antigens, do not have preformed antibodies to either of these. People with type O blood lack antigens A and B on their erythrocytes, but both anti-A and anti-B antibodies circulate in their blood plasma. Note that the Rh group is distinct from the ABO group, so any individual, no matter their ABO blood type, may have or lack this Rh antigen. When identifying a patient’s blood type, the Rh group is designated by adding the word positive or negative to the ABO type.This condition, known as hemolytic disease of the newborn (HDN) or erythroblastosis fetalis, may cause anemia in mild cases, but the agglutination and hemolysis can be so severe that without treatment the fetus may die in the womb or shortly after birth. Maternal anti-Rh antibodies may cross the placenta and enter the fetal bloodstream, causing agglutination and hemolysis of fetal erythrocytes. Since the introduction of RhoGAM in 1968, the incidence has dropped to about 0.1 percent in the United States. An unknown blood sample is allocated into separate wells. Into one well a small amount of anti-A antibody is added, and to another a small amount of anti-B antibody. If the antigen is present, the antibodies will cause visible agglutination of the cells (Figure 2). The blood should also be tested for Rh antibodies. The card contains three reaction sites or wells. One is coated with an anti-A antibody, one with an anti-B antibody, and one with an anti-D antibody (tests for the presence of Rh factor D). Mixing a drop of blood and saline into each well enables the blood to interact with a preparation of type-specific antibodies, also called anti-seras. For the purpose of transfusion, the donor’s and recipient’s blood types must match. That said, in emergency situations, when acute hemorrhage threatens the patient’s life, there may not be time for cross matching to identify blood type. Recall that type O erythrocytes do not display A or B antigens. Thus, anti-A or anti-B antibodies that might be circulating in the patient’s blood plasma will not encounter any erythrocyte surface antigens on the donated blood and therefore will not be provoked into a response. Also, introducing type O blood into an individual with type A, B, or AB blood will nevertheless introduce antibodies against both A and B antigens, as these are always circulating in the type O blood plasma. This may cause problems for the recipient, but because the volume of blood transfused is much lower than the volume of the patient’s own blood, the adverse effects of the relatively few infused plasma antibodies are typically limited. Rh factor also plays a role. Although it is always preferable to cross match a patient’s blood before transfusing, in a true life-threatening emergency situation, this is not always possible, and these procedures may be implemented. This patient can theoretically receive any type of blood, because the patient’s own blood—having both A and B antigens on the erythrocyte surface—does not produce anti-A or anti-B antibodies. However, keep in mind that the donor’s blood will contain circulating antibodies, again with possible negative implications. Figure 3 summarizes the blood types and compatibilities. In these circumstances, medics may at least try to replace some of the volume of blood that has been lost. This is done by intravenous administration of a saline solution that provides fluids and electrolytes in proportions equivalent to those of normal blood plasma. Research is ongoing to develop a safe and effective artificial blood that would carry out the oxygen-carrying function of blood without the RBCs, enabling transfusions in the field without concern for incompatibility. These blood substitutes normally contain hemoglobin- as well as perfluorocarbon-based oxygen carriers. See the text for more on the concept of a universal donor or recipient. In transfusion reactions, antibodies attach to antigens on the surfaces of erythrocytes and cause agglutination and hemolysis. ABO blood group antigens are designated A and B. People with type A blood have A antigens on their erythrocytes, whereas those with type B blood have B antigens. Those with AB blood have both A and B antigens, and those with type O blood have neither A nor B antigens. The blood plasma contains preformed antibodies against the antigens not present on a person’s erythrocytes. This is known as hemolytic disease of the newborn. Available from: 2013 The patient’s condition is critical, and there is no time for determining his blood type. What type of blood is transfused, and why? The technician collects a blood sample and performs a test to determine its type. She places a sample of the patient’s blood in two wells. To the first well she adds anti-A antibody. To the second she adds anti-B antibody. Both samples visibly agglutinate. Has the technician made an error, or is this a normal response. If normal, what blood type does this indicate. The advantages of FISH over in situ hybridization with radioactively labeled probes include spatial resolution, convenience, and speed. FISH techniques approach the sensitivity of autoradiographic techniques. Several schemes for probe modification and hybridization detection are described: biotinylated probe detected with fluorescently labeled avidin or antibiotin antibody, aminoacetylfluorene (AAF)-modified probe detected with an anti-AAF antibody, sulfonate-modified probe detected with an antisulfonate antibody, mercurated probe detected by a sulfhydryl group linked to either a fluorescent ligand or a hapten, which is detected with an antihapten antibody, and digoxigenin- labeled probes detected with an antidigoxigenin antibody. Biotin and digoxigenin moieties have been introduced in the probe through nick translation or random-primed polymerase reactions. Aminoacetylfluorene, sulfonate, and mercury have been introduced in the probe through simple chemical reactions. Published by Elsevier Inc. Recommended articles No articles found.