What is pneumonia? |

Causes and Symptoms

Although modern medicine succeeded several generations ago in identifying the key viruses and bacteria responsible for pneumonia and in developing efficient medications for its treatment, a surprisingly high number of deaths from the complications of pneumonia continue to occur. In large part this is the case because pneumonia, which involves infection and inflammation in the respiratory system, occurs not only on its own but also as a complication brought about by other serious illnesses. In aged patients, especially, general deterioration of the body’s resistance to bacterial or viral infection can lead in a final stage to death from pneumonia.

Just as the causes of pneumonia can vary, the disease itself may take different forms. Some sources postulate that pneumonia is not a single disease but a group of advanced lung inflammations. Because they are so similar in their symptoms and effects on the body, all members of this family of diseases are labeled as one form or another of pneumonia. Specific forms range from lobar pneumonia (caused by the bacterial invasion of Streptococcus pneumoniae into a single lobe of one lung) and bronchopneumonia (from Haemophilus influenzae bacteria colonizing in the bronchi) to viral pneumonia (which may be caused by complications originating from chickenpox or influenza virus). In all cases, symptoms include painful coughing, but other symptoms, such as high fever, reduced sputum production, or discolored (rust-tinged or greenish) sputum, may differ. It follows that the drugs that have been developed to treat pneumonia necessarily vary according to the variety of the disease involved.

Lobar pneumonia and bronchopneumonia are the two main classes of disease. The former occurs when an initial infection attacks only one lobe of one lung. Bronchopneumonia results from an initial inflammation in the bronchi and bronchioles (air passages to the lungs), which then spreads to the internal tissue of one or both lungs. Once the symptoms of pneumonia have become visible, any of the following may occur: fever, chills, shortness of breath, chest pains, or a painful cough that produces yellow-green or brownish sputum. These symptoms occur because of a condition called
pleurisy, which is an inflammation of the membrane lining the lungs themselves and the general chest cavity area.

Some assumptions about the causes of pneumonia being limited to bacterial or viral sources have been altered. In particular, clinical observation of patients suffering from AIDS reveals that certain fungi, yeasts, or protozoa can cause pneumonia in these and other cases where immunodeficiency disorders are present.

Although it is apparent that pneumococci can thrive in various parts of the bodies of animals, particularly monkeys and humans, the process that leads to general infection and a concentrated and dangerous attack on the pulmonary system has been the subject of many medical investigations. It is nearly certain that the presence of the
common cold virus in the upper respiratory tract can create the conditions needed for the movement of pneumococci from areas of the body where they may be generally present without causing harm (mainly in saliva) into the pulmonary system. Under conditions of normal health, many body mechanisms can stop a potential invasion of the pulmonary system. This process may involve nasal mucus, although it is not itself bactericidal (bacteria-killing), and other mucous membranes in the region of the larynx. Even beyond the larynx and vocal cords, mechanical means associated with the upward sweep of hairlike protrusions called cilia on the inner linings of deeper respiratory
membranes tend to protect the bronchial tree.

When normal protective processes are reduced, as when the cold virus is present, pneumococci may reach the lower respiratory zone and the parenchyma of the lung, where they settle and multiply. The metabolic products that accumulate as a result of this reproductive process begin to have injurious effects on the respiratory organs. Such injuries become actual lesions in the internal respiratory tissues. The process of infection that follows involves the deposition of fibrin in the adjacent blood and lymph vessels. This phenomenon actually tends to shield the invading organisms from the effects normally produced by antipneumococcal immune substances carried by the blood. If unchecked by medical treatment, reproduction of the invading pneumococci can lead to more extensive lesions. If tissue damage occurs, this can cause the formation of edema, a dangerous accumulation of fluids in spaces where fluids are not normally found. At a later stage of the disease, it appears that the pneumococci enter the interstitial and lymphatic tissues. The unchecked advance of pneumonia infection produces a general deterioration of vital breathing processes as excess fluids spread farther into the respiratory
system. In weakened or immunocompromised individuals, this process can lead to death.

Treatment and Therapy

Medical treatment of the two main types of pneumonia is not the same. Lobar pneumonia requires treatment with penicillin. Bronchopneumonia, although also caused by pneumococcus bacteria, must be treated with different
antibiotics. Most forms of pneumonia caused by viral infections, including psittacosis and mycoplasmal pneumonia, require one of two specific drugs: tetracycline or erythromycin. When viral pneumonia provides the basic disease to which bacterial infections in the lungs are added, however, antibiotics represent the main general means of treatment.

Since World War II, the progress of medical science in dealing with various types of pneumonia has been marked by the development of antimicrobial drugs that can be used in treating diagnosed cases of pneumonia. One of the earliest such drugs, which eventually turned out to be ineffective, was a derivative of quinine called Optochin. It was used for the first time on mice in 1912. Five years later, when the drug was applied to human patients, it was observed that the pneumococci were able to develop a surprising degree of resistance to these early antimicrobial substances. Thus, just as progress in the field of immunization had to wait for a later generation, so did effective drugs such as penicillin and other antibiotics that have become standard tools in the treatment of forms of pneumonia.

In most cases, advances in drug treatment to cure pneumonia have been strikingly successful. The phenomenon of the nonbacterial, nonviral version of Pneumocystis pneumonia arrived very soon after these successes. It posed a particular series of dilemmas for medical science in the 1980s and 1990s. This problem emerged when it became apparent that certain drugs that had been developed to treat pneumonia, in particular the drug combination of trimethoprim-sulfamethoxazole (TMP-SMZ), failed to achieve expected results in a rising number of cases of Pneumocystis pneumonia. This particular form of pneumonia turned out to be among the minority strains of the disease caused by single-celled microorganisms called protozoa.

The importance of P. carinii (also called P. jirovecii) in applied medical science soon extended beyond the restricted domain of pneumonia pathology. It had been discovered in 1909 in Brazil and was thought to affect only animals. This research involved local researchers led by the Italian Antonio Carini, whose name was attached to the discovery. It was only much later, in the 1940s and 1950s, that the presence of P. carinii could be traced to pneumonia in human infants. This meant that a relatively unusual form of pneumonia belonged to limited number of cases caused not by bacteria or viruses but by fungi, yeasts, or microorganisms, specifically, single-celled protozoa. This form of pneumonia remained a relatively rare occurrence until the number of AIDS cases increased.

What appeared to be a near epidemic frequency of P. carinii was in fact a marker or indicator for discovering patients suffering from AIDS. This observation made it possible to immediately test for the presence of AIDS whenever cases of P. carinii appeared. Clinical experience during the 1980s revealed that at least 60 percent of all persons suffering from AIDS had contracted or would contract P. carinii pneumonia. The presence of P. carinii is now assumed to be associated with AIDS unless that diagnosis is excluded by a laboratory test.

It is important to note that relatively rapid advances made by medical researchers in preventing the spread of P. carinii and in treating the cases that did occur among infants led to a new appreciation for pneumonia. Applied research dating from 1958 and extending into the 1970s produced surprisingly effective agents to combat P. carinii pneumonia. This work led to the early application of drugs to people infected with Human immunodeficiency virus (HIV). The concept of multiple drug therapy, patterned on TMP-SMZ, was also successfully applied in the field of cancer treatment.

Another drug, pentamidine, had been used to treat P. carinii pneumonia. When TMP-SMZ seemed to provide a superior treatment, pentamidine production was halted. When the potential utility of pentamidine in treating AIDS became apparent, the Centers for Disease Control and the Food and Drug Administration (FDA) had to take special action in 1984 to license an American supplier. This is how pentamidine quickly became widely available to treat individuals with AIDS. Pentamidine has also been successfully used as an effective treatment for a variety of viral diseases.

A side effect of these AIDS-related developments by the mid-1980s has been to reemphasize the importance of pneumonia. This renewed interest involves both treatments that are most appropriate for different types of pneumonia and research that is still needed to understand fully the role of this family of diseases in modern medicine and society.

Perspective and Prospects

Although modern medicine has not been able to reduce substantially or eliminate totally the number of cases of pneumonia, much has been learned about the disease and its causes. Scientific advances in the campaign to combat the effects of pneumonia in all areas of the world began with the first isolation of Streptococcus pneumoniae in France and the United States in 1880. The French discovery of pneumococci is associated with the laboratory of Louis Pasteur. Simultaneously, George Sternberg was completing work in the medical department of the US Army. In the first decade after the isolation of pneumococci, many different researchers contributed to laboratory findings that linked these bacteria to inflammatory infections in the lungs of animals. They extended their research to include the effects on humans.

One of the most important early breakthroughs came in 1884 when the Danish researcher Hans Christian Joachim Gram developed a laboratory method for identifying specific bacteria in tissue specimens. This technique, called Gram’s stain, revealed that different chemical reactions occur when samples of lung tissue and secretions from individuals ill with pneumonia and healthy persons are tested. The tissues stain very differently. The next step would lead to research into the phenomenon of phagocytosis, a process within pulmonary tissue that combats inapparent pneumococcus infection in healthy people. This specific discovery became linked with efforts to develop an immunization technology against pneumonia.

Until the 1980s, medical researchers used their knowledge of pneumonia mainly to develop methods of immunization against the disease. They also tried to diversify the drugs used in treating pneumonia. Efforts to produce a vaccine against pneumonia began with experiments by the German researchers George and Felix Klemperer, who tested antiserum in animals in 1891. The Klemperers were able to show that the offspring of adult rabbits which had been immunized were resistant to pneumococcal invasion and infection. Soon thereafter, they carried out the first injections of immune serum into human patients. This research ultimately led to the finding that there was no actual antitoxin or antibacterial property in the serum. Instead, it promoted phagocytosis, a process of encapsulation around pneumococci that aids in the immunological response of white blood cells in the body. The vaccine stimulates the body to create its own defenses.

In 1911 in South Africa, an experimental pneumonia vaccine program was undertaken. Although the specific program was not successful, the British physician and scientist Frederick Lister extended its theory. Unequivocal success with a pneumonia vaccine did not come until the last year of World War II. In 1945, C. M. MacLeod and several colleagues published research findings proving that pneumococcal infection in humans was preventable through the use of vaccines containing as many as fourteen specific antigens. These were termed capsular polysaccharides. The breakthrough that made those findings possible had been pioneered in 1930 when these antigens were injected into human beings for the first time. Previously, they had been used only in experiments with mice.

Pneumonia vaccines are critically important components of programs to prevent disease among older members of the population. In March 2013, the American Journal of Medicine published a study of 1,400 pneumonia patients over the age of fifty in which researchers found a correlation between pneumonia patients requiring hospitalization and an increased risk of decline their mental abilities. Experts recommend that the elderly receive a pneumonia vaccine each year. The death rate from pneumonia continues to rise, but not as quickly as the percentage of the population that is elderly. Pneumonia is one of the ten leading causes of death in the United States. In 1900, it was the second or third most common killer. Without vaccines, it might easily still be the second or third leading cause of death.

Children under the age of two are also at high risk for catching pneumonia. The World Health Organization reported in April 2013 that pneumonia was the leading cause of death in children worldwide, killing an estimated 1.2 million children younger than five each year. Only about 30 percent of the world's children with the disease receive antibiotics to treat it

Bibliography

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Badash, Michelle. "Pneumonia." Health Library, September 30, 2012.

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Karetzky, Monroe, Burke A. Cunha, and Robert D. Brandstetter. The Pneumonias. New York: Springer, 1993.

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Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow, eds. Current Medical Diagnosis and Treatment 2013. New York: McGraw-Hill Medical, 2012.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Streptococcus Pneumoniae Infections. San Diego, Calif.: Icon Health, 2002.

Pennington, James E. Respiratory Infections: Diagnosis and Management. 3d ed. Hoboken, N.J.: Raven Press, 1994.

Preidt, Robert. "HealthDay: Pneumonia May Lead to Serious Aftereffects for Seniors." MedlinePlus, March 22, 2013.

West, John B. Pulmonary Pathophysiology: The Essentials. 8th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2012.

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Why is Dave worried about his father coming to school in "Split Cherry Tree"?

In "Split Cherry Tree," Dave is anxious about his father's coming to the school because he will stand out as an anachronism at his school, and Dave fears he may "start something."

When Dave and his friends "broke down a cherry tree," their teacher, Professor Herbert, makes the boys pay for the tree; however, because Dave has no money, he has to remain after school and sweep in order to work off his debt. Having...

In "Split Cherry Tree," Dave is anxious about his father's coming to the school because he will stand out as an anachronism at his school, and Dave fears he may "start something."

When Dave and his friends "broke down a cherry tree," their teacher, Professor Herbert, makes the boys pay for the tree; however, because Dave has no money, he has to remain after school and sweep in order to work off his debt. Having to stay late causes Dave to raise his father's ire because he has to do Dave's chores along with his own work that he has done on their farm for that day. Dave fears telling his father why he has been late, knowing that his "Pa" will feel that Dave has been treated differently and unfairly from the other boys.

Just as Dave expects, his father is furious when he returns home late. When Dave tells his father that he has had to stay and work his dollar off after school, Pa wonders why Dave has been singled out--"Poor man's son, huh?"--and why the boys were in Eif Crabtree's orchard--"What kind of a school is it, nohow?" Then, as his father prepares to go to the school, threatening to "...straighten this thing out.... Luster Sexton says, "...a bullet will go in a professor same as it will any man."

Dave becomes extremely worried. Further, Pa accompanies him to school with a gun inside his coat, and Dave, who knows "Pa wouldn't be at home in the high school" with his overalls, big boots, and a sheepskin coat, fears what his father will do to his teacher. He is also embarrassed as Pa pulls out his gun and lays it on a seat in Professor Herbert's office. He is very worried that his father might strike his teacher.

His face was getting red. The red color was coming through the brown, weather beaten skin on Pa's face.

Fortunately, Professor Herbert maintains his composure and he explains well the circumstances of his making Dave work after school. Then, too, he demonstrates some of the things that the students are learning, and Pa is able to even teach Professor Herbert the benefits of a black snake. Later, Pa humbly admits that school has changed since his day.

What are oral contraceptives? How do they interact with other drugs?

Folate

Effect: Supplementation Possibly Helpful

Although the evidence is not consistent, women who are taking oral contraceptives
(OCs) may need extra folate. Because folate deficiency is
fairly common, even among women who are not taking OCs, and because the body
should not lack an essential nutrient, taking a folate supplement on general
principle is a good idea.

Other Nutrients

Effect: Supplementation Possibly Helpful

Evidence from several studies suggests that OCs might interfere with the absorption or metabolism of magnesium, vitamin B2, vitamin C, and zinc. With the exception of the trials involving magnesium, these studies used older, high-dose OCs. Modern, low-dose OCs may not affect nutrients to the same extent.

St. John’s Wort

Effect: Decreased Effectiveness of Drug

Reliable case reports, as well as controlled clinical trials, indicate that
St. John’s
wort interferes with the effectiveness of oral contraceptives
and may have led to unwanted pregnancies.

Indole-3-Carbinol

Effect: Possible Reduced Effectiveness of Drug

Indole-3-carbinol
(I3C) is a substance found in broccoli that is thought to
have cancer-preventive effects. One of its mechanisms of action is thought to
involve facilitating the inactivation of estrogen, as well as blocking its effects
on cells. The net result could be decreased effectiveness of oral
contraceptives.

Dong Quai, St. John’s Wort

Effect: Possible Harmful Interaction

OCs have been reported to cause increased sensitivity to the sun, amplifying the
risk of sunburn or skin rash. Because dong quai and St. John’s wort may also
cause this problem, taking these herbal supplements while taking OCs might add to
this risk. It may be a good idea to wear sunscreen or protective clothing during
sun exposure if one takes one of these herbs while using OCs.

Rosemary

Effect: Possible Harmful Interaction

Weak evidence hints that the herb rosemary may enhance the liver’s
ability to deactivate estrogen in the body. This could potentially interfere with
the activity of medications that contain estrogen.

Grapefruit Juice

Effect: Possible Harmful Interaction

Grapefruit juice slows the body’s normal breakdown of several drugs, including estrogen, allowing it to build up to potentially excessive levels in the blood. A recent study indicates this effect can last for three days or more following the last glass of juice. If one takes estrogen, the safest approach is to avoid grapefruit juice altogether.

Resveratrol

Effect: Possible Harmful Interaction

The supplement resveratrol has a chemical structure similar to that of the
synthetic estrogen diethylstilbestrol and produces estrogenic-like effects. For
this reason, it should not be combined with prescription estrogen products.

Milk Thistle

Effect: Possible Decreased Action of Drug

One report has noted that an ingredient of milk thistle,
silibinin, can inhibit a bacterial enzyme called beta-glucuronidase. This enzyme
helps oral contraceptives work. Taking milk thistle could, therefore, reduce the
effectiveness of OCs.

Androstenedione

Effect: Theoretical Harmful Interaction

Androstenedione has become popular as a sports supplement,
on the theory that it increases testosterone levels, as well as sports
performance. However, there is no evidence that it is effective. In addition,
androstenedione appears more likely to elevate estrogen than testosterone levels.
This could increase risks of developing estrogen-related diseases, including
breast and uterine cancers. Women taking estrogen should not take
androstenedione.

Soy

Effect: Probably No Interaction

Fears have been expressed by some experts that soy or soy
isoflavones might interfere with the action of oral
contraceptives. However, one study of thity-six women suggests that such concerns
are groundless.

Bibliography

Bradlow, H. L., et al. “Multifunctional Aspects of the Action of Indole-3-Carbinol as an Antitumor Agent.” Annals of the New York Academy of Sciences 889 (1999): 204-13.

Jobst, K. A., et al. “Safety of St. John’s Wort (Hypericum perforatum).” The Lancet 355 (2000): 575.

Martini, M. C., et al. “Effects of Soy Intake on Sex Hormone Metabolism in Premenopausal Women.” Nutrition and Cancer 34 (1999): 133-139.

Meng, Q., et al. “Indole-3-Carbinol Is a Negative Regulator of Estrogen Receptor-Alpha Signaling in Human Tumor Cells.” Journal of Nutrition 130 (2000): 2927-2931.

Michnovicz, J. J. “Increased Estrogen 2-Hydroxylation in Obese Women Using Oral Indole-3-Carbinol.” International Journal of Obesity and Related Metabolic Disorders 22 (1998): 227-229.

Pfrunder, A., et al. “Interaction of St. John’s Wort with Low-Dose Oral Contraceptive Therapy.” British Journal of Clinical Pharmacology 56 (2003): 683-690.

Takanaga, H., et al. “Relationship Between Time After Intake of Grapefruit Juice and the Effect on Pharmacokinetics and Pharmacodynamics of Nisoldipine in Healthy Subjects.” Clinical Pharmacology and Therapeutics 67 (2000): 201-214.

What is the relationship between birth defects and alcohol?

The Dangers of Drinking for Two

When a pregnant woman drinks alcoholic beverages, the alcohol in her blood crosses the placenta easily and enters the embryo or fetus through the umbilical cord. Children affected by prenatal exposure to alcohol may suffer lifelong consequences, including intellectual impairment, learning disabilities, and serious behavioral problems.

All drinks containing alcohol can hurt an unborn baby. A standard twelve-ounce can of beer has the same amount of alcohol as a four-ounce glass of wine or a one-ounce shot of straight liquor. In addition, some alcoholic drinks, such as malt beverages, wine coolers, and mixed drinks, often contain more alcohol than a twelve-ounce can of beer. Studies have not been done to establish a known safe amount of alcohol that a woman can drink while pregnant.

Any time a pregnant woman participates in regular drinking increases her chance of having a miscarriage and puts her unborn child at risk for growth deficiencies, learning disabilities, and behavioral problems. Birth defects associated with prenatal exposure to alcohol can occur in the first eight weeks of pregnancy, before a woman even knows that she is pregnant.

Between 2011 and 2013, one in ten pregnant women surveyed reported alcohol use, and one in thirty-three reported binge drinking within thirty days of the survey, according to the CDC.

Fetal Alcohol Syndrome

Fetal alcohol syndrome (FAS) is caused by alcohol consumption during pregnancy and is one of the leading known causes of mental disability and birth defects. It is characterized by abnormal facial features, including small head size, narrow eye slits, and abnormalities of the nose and lip areas; growth deficiencies; and problems with the central nervous system (CNS).

Children with FAS may have problems with learning, memory, attention span, problem solving, speech, and hearing. These problems often lead to difficulties in school and in getting along with others. FAS is an irreversible condition that affects every aspect of a child’s life and the lives of his or her family. FAS is preventable if a woman abstains from alcohol while she is pregnant.

Fetal Alcohol Effects

In the past, the term fetal alcohol effects (FAE) was generally used to describe children who did not have all of the clinical signs of FAS, but who had various problems, including growth deficiency, behavioral problems, or problems with motor and speech skills. FAE has also been used to describe children who have all of the diagnostic features of FAS, but at mild levels. Because experts in the field were unable to agree on a single definition for FAE, the Institute of Medicine (IOM) proposed the terms alcohol-related neurodevelopment disorder (ARND) and alcohol-related birth defects (ARBD). ARND describes the functional or mental impairments linked to prenatal alcohol exposure, such as behavioral or cognitive abnormalities. These include learning difficulties, poor school performance, poor impulse control, and problems with mathematical skills, memory, attention, and judgment. ARBD describes malformations of the skeletal system and major organ systems. Such malformations may include defects of the heart, kidneys, bones, and auditory system.

Treatment and Prevention

There is no cure for either fetal alcohol syndrome or fetal alcohol effects. They are irreversible, lifelong conditions that affect every aspect of a child’s development. With early identification and diagnosis, a child with FAS can receive services that can help to maximize his or her potential.

The easiest way to prevent FAS is to abstain from alcohol use during pregnancy. Any amount of alcohol consumed during pregnancy is potentially dangerous to an unborn baby. If a pregnant woman is drinking during pregnancy, it is never too late for her to stop. The sooner a woman quits drinking, the better it will be for both her and her baby. If a woman is not able to quit drinking, she should contact her local social service agency or health plan for alcohol abuse treatment, if needed. If a woman is not yet pregnant, she should use an effective form of birth control until her drinking is under control.

Mothers are not the only ones who can help prevent FAS, however. Significant others, family members, schools, social organizations, and communities alike can help to prevent FAS through education and intervention. Also, emerging research suggests that long-term alcohol abuse among men may alter sperm cells in ways that introduce defects to the fetus at conception. Continued research will help to clarify this link and improve prevention efforts.

Bibliography

Chaudhuri, J. D. “Alcohol and the Developing Fetus—A Review.” Medical Science Monitor 6.5 (2000): 1031–41. Print.

“Drinking Alcohol During Pregnancy.” March of Dimes. March of Dimes Foundation, Nov. 2008. Web. 29 Mar. 2012.

“Drinking and Your Pregnancy.” NIAAA. Natl. Inst. on Alcohol Abuse and Alcoholism, May 2010. Web. 29 Mar. 2012.

"Fetal Alcohol Spectrum Disorders (FASDs): Data and Statistics." Centers for Disease Control and Prevention. CDC, 24 Sept. 2015. Web. 28 Oct. 2015

Nayak, Raghavendra B., and Pratima Murthy. “Fetal Alcohol Spectrum Disorder.” Indian Pediatrics 45.12 (2008): 977–83. Print.

“Prenatal Exposure to Alcohol.” Alcohol Research & Health 24.1 (2000): 32–41. Print.

Thackray, Helen M., and Cynthia Tifft. “Fetal Alcohol Syndrome.” Pediatrics in Review 22 (2001): 47–55. Print.

“Treating Individuals Affected with FASD.” NOFAS. Natl. Org. on Fetal Alcohol Syndrome, 2004. Web. 29 Mar. 2012.

How does a social support system affect mental health?

Introduction

Social support is a pervasive phenomenon spanning people’s relationships throughout their lives. In everyday life, particularly in times of distress, people convey a need for support from relatives, friends, partners, coworkers, or other members of their social community. This powerful inclination to seek and provide support is thought to have adaptive evolutionary significance because interdependency may enhance the likelihood of survival, especially when under threat of predation. The human response to seek the presence of others in the aftermath of natural disasters or other trauma testifies to the need for and benefits of social affiliation. Research suggests that social support is sought to such an extent because it is an effective method of coping with stress and may protect against potential adverse mental health consequences.

A primary psychological need to belong may underlie the tendency to turn to others under demanding circumstances. In support of this possibility, aside from fostering adjustment to stressful and demanding events, a sufficient quantity and quality of support are essential for optimal functioning in daily life. It is important that social contact is regular, positive, and meaningful, and that interaction is perceived as having the potential for disclosure of private and sensitive feelings. The need to belong may compel people to provide this kind of emotional support or more tangible assistance to those with whom they have formed interpersonal attachments. Indeed, the theoretical literature has proposed several types of social support in a bid to form a taxonomy of support and to detail the situations in which various types of social support are most effective.

Instrumental and Emotional Social Support

The numerous ways that supportive people can help others have been categorized broadly as either instrumental or emotional in focus. Instrumental support involves the provision of direct, pragmatic assistance aimed at solving problems. This can be by passing on information to facilitate better understanding of a stressful event, by helping to remove obstacles or counteract losses and harm, or by providing goods or financial assistance. Instrumental assistance can reduce the impact of a stressor by promoting effective coping strategies through the distribution of information and by facilitating protective action through the supply of tangible resources. Emotional support, in contrast, is aimed at the person instead of the objective problem or stressor. It may include helping the person escape from negative emotions and feel better, conveying warmth and affection, reaffirming a commitment to a nurturing relationship, talking about emotions, listening to what the suffering person wants to say, and in general encouraging the other person to feel loved, cared for, and valued.

Evidence within the social support literature is mixed as to whether instrumental or emotional support is more important for mental health. In 1999, Chockalingam Viswesvaran and colleagues conducted a meta-analysis of social support studies focusing on work situations and found emotional support to be more predictive of good outcomes following stressful experiences. Instrumental support may have a closer relationship with physical health, as demonstrated by Viveca Östberg and Carin Lennartsson, who found economic support to be more predictive than emotional support of good physical health. Emotional support may potentially capture the essence of social support more completely than instrumental support, insofar as it contributes to feeling worthwhile, competent, and esteemed as a member of a group. However, substantial overlap is typically observed in the measurement of both types of support. This may reflect the emotional meaning of instrumental support and how certain emotions facilitate action. For example, information may relieve emotional concerns such as worry and anxiety, and positive emotion may promote problem-solving behavior.

Therefore, although a taxonomy of social support strategies is useful, the distinction between types is by no means absolute, and instrumental and emotional support may interact. As is apparent in the definition of social support, it is important to recognize that it is not enough that support is in place, but rather that the perception or experience of that assistance is required for effects to occur.

Experience of Social Support

Considerable reassurance can be found in simply knowing that one is cared for and that support is available from others in times of distress. Implicit social support refers to the emotional comfort derived from social networks without explicit discussion of problems or stressful events. The perception of social support is the comfort of implicit social support combined with the belief that others can be relied on to provide care and solace when needed. This perception has been shown not to coincide exactly with the actual amount of instrumental or emotional support that one receives. In fact, perceived available social support can be beneficial in reducing stress even if support is not actually used. Sheldon Cohen and S. Leonard Syme in 1985, and several researchers since, have provided evidence that beliefs about the availability of social support are more closely related to mental health than received support. The critical importance of subjective perceptions of social support opens up the question as to what psychological factors may condition how support is viewed.

The extent to which a person feels affective concern from others may be substantially related to factors such as personality, attachment style, and various needs and goals. For instance, Nancy Collins and Brooke Feeney in 2004 showed the construal of supportive interaction to vary as a function of the participant’s attachment style. Insecure attachment is characterized by a diminished expectation that others will be emotionally available and responsive when needed. Such anxious or avoidant people rated messages sent by an assigned partner in a stressful task as less supportive than did securely attached people. The divergence between the support that insecurely attached people feel they need and the support they perceive to be available has been linked to early experiences with parents or other attachment figures. Such experiences are thought to negatively influence both the construal of social support and the cultivation of supportive relationships by enhancing the salience of potential rejection and stimulating avoidance behaviors.

The urge to approach rather than avoid others has been linked to positive emotion, which functions to broaden momentary thought-action repertoires and build personal resources. In the context of social support, considering the well-being of others and having compassionate goals has been shown to build support over time. Jennifer Crocker and Amy Canevello in 2008 demonstrated compassionate goals to increase perceived social support, connectedness, and trust over a ten-week period in first-semester college students. Goals are thought to condition the development of one’s support system. This occurs positively when the focus of the relational goal is on supporting others and responding to their needs rather than obtaining something for the self (for example, promoting a desired self-image through one’s relationships). In this way, responsiveness is reciprocated even though this is not the primary goal of support offered out of compassion.

Protective Role of Social Support

In 1995, Roy Baumeister and Mark Leary proposed that humans have a fundamental need to belong, and that a sufficient quantity of stable interpersonal relationships characterized by affective concern is essential for optimal levels of well-being in daily life. Integration in a social network characterized by mutual obligation and the perception that one is loved and cared for can have ameliorative effects on mental health through promoting a stream of positive feelings, a sense of stability, and a perception that one has a worthwhile role in the community. Evidence supporting the beneficial effects of social integration has been detailed by Sheldon Cohen and Thomas A. Wills, who describe a main effect model of social support. In this model, social integration can enhance well-being without improving the capacity for coping with stressful events. However, the authors show that another form of social support, perceived available support, protects against the effects of stressful events, thus mitigating the relationship between stressors and the development of mental illness. This stress-buffering model has led to the proposition that deficits in social support enhance the risk for depression, alcoholism, anxiety, and psychosomatic symptoms. Michael Windle in 1992 showed that parental social support, but not peer support, had beneficial stress protective effects. Similarly, Eric Stice and colleagues, in a 2004 prospective study, demonstrated that deficits in parental but not peer support were related to a worsening of depressive symptoms over time and an increased likelihood of the onset of major depression.

As well as the source of social support, there is evidence to suggest that the type and degree of explicitness of support are important factors in determining the effect of the support provided. Stephanie Brown and colleagues in 2003 found that providing social support to others can be more beneficial to health and well-being than receiving support, and can even reduce the risk of mortality. Actively supporting others may reinforce existing relationships, provide a sense of meaning, and fortify the belief that one is esteemed and matters to others. Explicit acts of support may have potential costs to the recipient, such as leading to perceptions of being a burden, and feelings of stress, guilt, and indebtedness. Support may be most effective when responsiveness is subtle and the receiver is unaware of the explicit action of the support network. For example, when stressful decisions are being made regarding college course selection, job changes, or resolving interpersonal problems, explicit advice from multiple and potentially conflicting sources can interfere with decision making and cause additional stress. Less visible emotional support may reduce the distress associated with major life changes or threatening situations. It is also imperative that there is a suitable match between the support provider and the type of support provided. During times of stress, emotional support may be best received from an intimate partner or one’s immediate family, whereas information and advice may be more welcomed from an expert.

Bibliography

Baumeister, Roy F., and Mark R. Leary. “The Need to Belong: Desire for Interpersonal Attachments as a Fundamental Human Motivation.” Psychological Bulletin 117.3 (1995): 497–529. Print.

Brown, Stephanie, Randolph M. Nesse, Amiram D. Vinokur, and Dylan M. Smith. “Providing Social Support May Be More Beneficial than Receiving It: Results from a Prospective Study of Mortality.” Psychological Science 14.4 (2003): 320–27. Print.

Bruhn, John G. The Sociology of Community Connections. New York: Springer, 2011. Print.

Cohen, Sheldon, and Thomas A. Wills. “Stress, Social Support, and the Buffering Hypothesis.” Psychological Bulletin 98.2 (1985): 310–57. Print.

McDonnell, Roberta. Creativity and Social Support in Mental Health. New York: Palgrave, 2014. Print.

Roy, Ranjan. Social Support, Health, and Illness. Toronto: U of Toronto P, 2011. Print.

Stice, Eric, Jennifer Ragan, and Patrick Randall. “Prospective Relations Between Social Support and Depression: Differential Direction of Effects for Parent and Peer Support.” Journal of Abnormal Psychology 113.1 (2004): 155–59. Print.

Taylor, Shelley. “Social Support.” Foundations of Health Psychology. Ed. Howard S. Friedman and Roxane C. Silver. New York: Oxford UP, 2006. Print.

How does Robert Frost try to bring out the sadness of the boy's death in "Out, Out--"?

The title of the poem is a reference or an allusion to the play Macbeth. Upon learning of his wife's death, Macbeth talks about how fleeting and meaningless life is: 

Out, out brief candle, 

Life's but a walking shadow, a poor player 

That struts and frets his hour upon the stage 

And then is heard no more. It is a tale 

Told by an idiot, full of sound and fury, 

Signifying nothing. (V.v.25-30) 

In...

The title of the poem is a reference or an allusion to the play Macbeth. Upon learning of his wife's death, Macbeth talks about how fleeting and meaningless life is: 

Out, out brief candle, 

Life's but a walking shadow, a poor player 

That struts and frets his hour upon the stage 

And then is heard no more. It is a tale 

Told by an idiot, full of sound and fury, 

Signifying nothing. (V.v.25-30) 

In the poem, the boy dies too young. His life was much too "brief." The speaker in the poem wishes the boy had been given a break.

"Call it a day, I wish they might have said / To please the boy by giving him the half hour / That a boy counts so much when saved from work."

The boy is doing "a man's work." The speaker implies that, ideally, the boy should be playing or doing a boy's work. Unfortunately, the family needs the boy to work. So, his life is cut short and because he had to work, he has lost a significant portion of his childhood. 

There are more obvious attempts at empathy. The boy's cries not to have his hand cut off are powerful. The boy dies and the family returns "to their affairs." Here, the speaker is being very critical. The boy is dead and there is no mention of the grieving process. They simply go on with what they had been doing. The boy's shortened life is sad to begin with. The indifferent reactions of those around him make his life/death seem more sad and less meaningful. This is the connection to the quote from Macbeth. 

Is the boy's death simply a random part of nature? And if it is random, does that make it more senseless? Or is it a result of humanity's growing obsession with technology (the saw)? Frost does not answer these questions about death. He leaves it for the reader to decide. For some, this lack of closure adds to the meaninglessness and perhaps adds to the sadness of the poem. 

What is kyphosis? |

Causes and Symptoms

Patients with kyphosis appear to be looking down with their shoulders markedly bent forward. They are unable to straighten their backs and their body height is reduced, causing their arms to appear to be disproportionately long. The increased curvature of the thoracic vertebrae tilts the head forward, and the patient has to raise his or her head and hyperextend his or her neck in order to look forward. This posture increases the strain on the neck muscles and leads to discomfort in the neck, shoulders, and upper back. It limits the field of vision and increases the patient’s chances of tripping over an object not directly in the line of vision. It also shifts forward the body’s center of gravity and increases the chances of falling.

In severe cases, kyphosis limits chest expansion during breathing. As a result, less air gets into the lungs, which become underventilated and prone to infections. Pneumonia
is a common cause of death in these patients. In very severe cases, the curvature of the thoracic vertebrae is so pronounced that the lower ribs lie over the pelvic cavity. Patients with severe kyphosis are not able to lie flat on their backs, and many spend most of their time sitting up in a chair or in bed, propped by a number of pillows. Unless the patient changes positions frequently, the pressure exerted by the vertebrae on the skin and subcutaneous tissue may precipitate pressure sores (bedsores)
on the upper back. Pressure sores may also develop on the buttocks. The sores often become infected, and the infection may spread to the blood, leading to septicemia and death.

The most common cause of kyphosis is osteoporosis, a disease in which the bone mass is reduced. As a result, the bones become mechanically weak and are unable to sustain the pressure of the body weight. The vertebrae gradually become wedged and partially collapsed, more so in the front (anteriorly) than in the back (posteriorly), thus increasing the forward curvature of the thoracic vertebrae. Sometimes, the compression of a vertebra is associated with sudden, very severe and incapacitating pain that is usually relieved spontaneously after about four weeks. In most cases, however, the compression is a gradual process associated with slowly worsening back discomfort. The discomfort is caused by the strain imposed on the muscles on either side of the vertebrae. In rare instances, the nerves exiting the spinal cord become trapped by the wedged or collapsed vertebrae, and the patient experiences severe pain that tends to radiate to the area supplied by the entrapped nerve.

Less common causes of kyphosis include the compression of a vertebra as a result of tumors or infections. In these cases, the angulation of the thoracic curvature is very prominent.

Treatment and Therapy

The availability of medications to treat and prevent osteoporosis, including alendronate and teriparatide, should significantly reduce the prevalence of both that disease and kyphosis. Severe cases of kyphosis or cases due to infection or tumor may require surgery.

Bibliography

Byyny, Richard L., and Leon Speroff. A Clinical Guide for the Care of Older Women: Primary and Preventive Care. 2d ed. Baltimore: Williams & Wilkins, 1996.

Currey, John D. Bones: Structures and Mechanics. 2d ed. Princeton, N.J.: Princeton University Press, 2006.

Heaney, Robert P. “Osteoporosis.” In Nutrition in Women’s Health, edited by Debra A. Krummel and Penny M. Kris-Etherton. Gaithersburg, Md.: Aspen, 1996.

Hodgson, Stephen F., ed. Mayo Clinic on Osteoporosis: Keeping Bones Healthy and Strong and Reducing the Risk of Fractures. Rochester, Minn.: Mayo Clinic, 2003.

Joseph, Thomas N., and David Zieve. “Kyphosis.” MedlinePlus, September 4, 2012.

Meredith, C. M. “Exercise in the Prevention of Osteoporosis.” In Nutrition of the Elderly, edited by Hamish Munro and Gunter Schlierf. Nestle’s Nutrition Workshop Series 29. New York: Raven Press, 1992.

Nelson, Miriam E., and Sarah Wernick. Strong Women, Strong Bones: Everything You Need to Know to Prevent, Treat, and Beat Osteoporosis. Rev. ed. New York: Berkley Books, 2006.

Van De Graaff, Kent M. Human Anatomy. 6th ed. New York: McGraw-Hill, 2002.

What are bioethics in genetics?

The Emergence of Bioethics

As early as the mid-1960s, advances in genetics and reproduction, life support, and transplantation technologies spurred an increased focus on ethical issues in medicine and scientific research. From the late 1960s through the mid-1970s, bioethicists were preoccupied with the moral difficulties of obtaining voluntary, informed consent from human subjects in scientific research. They concentrated on the development of ethical guidelines in research that would ensure the protection of individuals vulnerable to exploitation, including mentally or physically handicapped individuals, prisoners, and children. Beginning in the mid-1970s and continuing through the mid-1980s, bioethicists became increasingly involved in discussions of the definitions of life, death, and what it means to be human. In the mid-1980s, practitioners began to focus on cost containment in health care and the allocation of scarce medical resources.

Beginning in 1992, the Joint Commission on Accreditation of Health Care Organizations, the US agency that accredits hospitals and health care institutions, required these organizations to establish committees to formulate ethics policies and address ethical issues. Ethics teams within hospitals and professional organizations exist to provide consultation regarding ethical dilemmas in clinical practice and research. Such resources are critical as technological advances, particularly related to genetics and genomics, proceed more rapidly than policy. Centers for the study of biomedical ethics such as the American Society for Bioethics and Humanities are important forums for public debate and research. Since completion of the Human Genome Project, an increasing number of organizations are committed to ethical research and policy making related to the use of genomic information.

The overriding principle of bioethics and US law is to respect each person’s right to make decisions, free of coercion, about treatments or procedures he or she will undergo. This principle is complicated when the person making the decision is considered incompetent because of youth, intellectual disability, or medical deterioration. Other important principles include a patient’s right to know that medical practitioners are telling the truth, the right to know the risks and benefits of proposed medical treatment, and the right to privacy of health information.

Impact and Applications

Advances in genomics and genetic testing have presented numerous dilemmas for bioethicists, patients, and health care providers. For example, as the ability to forecast and understand the genetic code progresses, people will have to decide whether knowing the future, even if it cannot be altered or changed, is beneficial to them or their children. Knowledge of the genomic basis of common diseases has lead to the birth of direct-to-consumer marketing of testing that provides individuals with often complicated risk profiles for conditions such as diabetes and heart disease. Bioethicists are critical players in policy-making regarding this new form of personalized medicine.

Bioethicists help people determine the value of genetic testing, including the risks and benefits of genetic testing in particular situations. Factors typically considered before a person undergoes genetic testing include the nature of the test, the timing of the test, and the impact that the results will have on health and medical management. Testing can be done prenatally to detect disorders in fetuses; it can also be done before conception to determine whether a prospective parent is a carrier for a particular disorder or disease that could be passed to a child. Technology even allows for testing of embryos created by in vitro fertilization, thereby preventing the transmission of a genetic condition by transferring only unaffected embryos to the mother’s womb. Predictive and presymptomatic genetic tests can provide information about whether an adult has an increased susceptibility to, or will ultimately manifest symptoms of, a genetic disorder. Information gained from genetic testing could help predict the nature and severity of a particular disorder as well as potential options for screening or intervention. Knowing one’s genetic fate may be more of a burden than a person wants, however, particularly if nothing can be done to change or alter the risks that the person faces. Bioethicists act as guides through the complicated and often wrenching decision process.

Consumers of genetic testing must also decide whether the knowledge gained from the test is worth potential legal and social implications. In 2008, the Genetic Information Nondiscrimination Act (GINA) was signed into law. GINA provides protection against genetic discrimination in health insurance and employment, but it does not protect other insurance arenas, such as life insurance and disability insurance. Fear of discrimination may prevent some individuals from pursuing genetic testing that could provide beneficial guidance for preventive care. For example, a woman with a strong family history of breast cancer could have genetic testing to determine if she has inherited a hereditary cancer predisposition syndrome, which in turn would lead to increased vigilance with breast screening. Many women in this situation defer testing because of discrimination fears and risk detection of cancer at a much later stage, with potentially devastating consequences. Bioethicists can help guide policymakers in creating stricter protections against potential discrimination.

The Human Genome Project has provided researchers with a wealth of information, but this comes with a paucity of knowledge about the specific effects of the genetic sequence related to health and disease. Genome-wide association studies are ongoing to better understand the complicated nature of gene-gene and gene-environment interactions. In 2007, the first individual genome was sequenced, that of biologist Craig Venter, and the cost for individuals to sequence their own genomes has lowered consistently and significantly, from $2.7 billion in 2003 to around $1,000 in 2014. However, the challenge to bioethicists, researchers, and the general public is how to interpret the information in a meaningful way.

Key terms




genetic testing


:

the use of the techniques of genetics research to determine a person’s risk of developing, or status as a carrier of, a disease or other disorder





informed consent


:

the right of patients to know the risks of medical treatment and to determine what is done to their bodies





Bibliography

Beauchamp, Tom, et al. Contemporary Issues in Bioethics. 8th ed. Belmont: Thomson/Wadsworth, 2014. Print.

Bulger, Ruth Ellen, Elizabeth Heitman, and Stanley Joel Reiser, eds. The Ethical Dimensions of the Biological and Health Sciences. 2nd ed. New York: Cambridge UP, 2002. Print.

Caplan, Arthur. Due Consideration: Controversy in the Age of Medical Miracles. New York: Wiley, 1997. Print.

Chadwick, Ruth F., Mairi Levitt, and Darren Shickle. The Right to Know and the Right Not to Know: Genetic Privacy and Responsibility. New York: Cambridge UP, 2014. Print.

Charon, Rita, and Martha Montello, eds. Stories Matter: The Role of Narrative in Medical Ethics. New York: Routledge, 2002. Print.

Comstock, Gary L., ed. Life Science Ethics. 2nd ed. New York: Springer, 2010. Print.

Danis, Marion, Carolyn Clancy, and Larry R. Churchill, eds. Ethical Dimensions of Health Policy. New York: Oxford UP, 2002. Print.

Evans, John Hyde. Playing God? Human Genetic Engineering and the Rationalization of Public Bioethical Debate. Chicago: U of Chicago P, 2002. Print.

Kass, Leon R. Life, Liberty, and the Defense of Dignity: The Challenge for Bioethics. San Francisco: Encounter, 2002. Print.

Kristol, William, and Eric Cohen, eds. The Future Is Now: America Confronts the New Genetics. Lanham: Rowman, 2002. Print.

Langlois, Adèle. Negotiating Bioethics: The Governance of UNESCO’s Bioethics Programme. New York: Routledge, 2013. Print.

May, Thomas. Bioethics in a Liberal Society: The Political Framework of Bioethics Decision Making. Baltimore: Johns Hopkins UP, 2002. Print.

Mepham, Ben. Bioethics: An Introduction for the Biosciences. New York: Oxford UP, 2008. Print.

O’Neill, Onora. Autonomy and Trust in Bioethics. New York: Cambridge UP, 2002. Print.

Sandler, Ronald L., John Basl. Designer Biology: The Ethics of Intensively Engineering Biological and Ecological Systems. Lanham: Lexington, 2013. Print.

Singer, Peter. Unsanctifying Human Life: Essays on Ethics. Ed. Helga Kuhse. Malden: Blackwell, 2002. Print.

Veatch, Robert M. The Basics of Bioethics. 3rd ed. Upper Saddle River: Prentice, 2012. Print.

Widdows, Heather. The Connected Self: The Ethics and Governance of the Genetic Individual. New York: Cambridge UP, 2013. Print.

What is a macrobiotic diet? Does it help to fight cancer?

History: The word “macrobiotic” comes from the Greek words for “great life” and was first used by Hippocrates, the father of medicine. In the eighteenth century, German physician Christoph Hufeland to used this term describe a program for good health. The modern macrobiotic diet was developed in the twentieth century by George Ohsawa and has evolved under Michio Kushi. It was further popularized in the 1980s when a number of books were published including books by several medical professionals who credited the diet for their recovery from cancer and other illnesses.

The diet: On a typical day, the standard macrobiotic diet includes complex carbohydrates from brown rice, millet, barley, whole wheat, oats, and other whole grains (50 to 60 percent of calories), vegetables and fruit (20 to 25 percent of calories), beans and bean products (such as tofu), sea vegetables, and vegetable oil. Fish or seafood, nuts and seeds, pickles, and sweets are eaten occasionally (once a week). Consumption of red meat, eggs, poultry, and dairy are discouraged, as are tropical fruits, refined sugars, alcohol, and caffeinated beverages. The diet is modifiable based on a person’s age, sex, activity level, personal needs, and environment.

Benefits: Little research has been done on the macrobiotic diet for cancer prevention, and most of the research to date has been inconclusive. The diet may affect hormone metabolism; for example, women consuming a macrobiotic diet have much higher levels of phytoestrogens (hormone-like plant compounds) in their urine than women consuming an omnivorous diet. This may result in a lower risk for hormonally influenced cancers (such as breast cancer). In addition, the macrobiotic diet is consistent with general cancer prevention guidelines of reducing fat intake, animal products, and processed foods while increasing intake of whole grains, vegetables, and fruits.

Risks: In the late 1980s, there were reports that children and adolescents eating a macrobiotic diet showed below-average growth and vitamin B12 and vitamin D deficiency. Most dietitians recommend that people on macrobiotic and vegan diets make sure to get enough vitamin B12
and vitamin D from fortified foods or supplements. Other concerns include lack of protein, inadequate calcium intake, and dehydration.

Adams, Maria. "The Macrobiotic Diet." Health Library. EBSCO, Sept. 2013. Web. 21 Oct. 2014.

Cassileth, Barrie R. "Macrobiotics." The Complete Guide to Complementary Therapies in Cancer Care: Essential Information for Patients, Survivors and Health Professionals. Singapore: World Scientific, 2011. Digital file.

Hechtman, Leah. Clinical Naturopathic Medicine. Chatswood: Elsevier Australia, 2012. Print.

Kushi, Michio, and Alex Jack. The Cancer Prevention Diet: The Macrobiotic Approach to Preventing and Relieving Cancer. Rev. and updated 25th anniversary ed. New York: St. Martin's, 2009. Print.

"Macrobiotic Diet." Cancer.org. Amer. Cancer Soc., 1 Nov. 2008. Web. 21 Oct. 2014.

What are genomic libraries? |

What Is a Genomic Library?

Scientists often need to search through all the genetic information present in an organism to find a specific gene. It is thus convenient to have collections of genetic sequences stored so that such information is readily available. These collections are known as genomic libraries.

The library metaphor is useful in explaining both the structure and function of these information-storage centers. If one were interested in finding a specific literary phrase, one could go to a conventional library and search through the collected works. In such a library, the information is made up of letters organized in a linear fashion to form words, sentences, and chapters. It would not be useful to store this information as individual words or letters or as words collected in a random, jumbled fashion, as the information’s meaning could not then be determined. The more books a library has, the closer it can come to having the complete literary collection, although no collection can guarantee that it has every piece of written word. The same is true of a genomic library. The stored pieces of genetic information cannot be individual bits but must be ordered sequences that are long enough to define a gene. The longer the string of information, the easier it is to make sense of the gene they make up, or “encode.” The more pieces of genetic information a library has, the more likely it is to contain all the information present in a cell. Even a large
collection of sequences, however, cannot guarantee that it contains every piece of genetic information.

How Is a Genomic Library Created?

In order for a genomic library to be practical, some method must be developed to put an entire genome into discrete units, each of which contains sufficiently large amounts of information to be useful but which are also easily replicated and studied. The method must also generate fragments that overlap one another for short stretches. The information exists in the form of chromosomes composed of millions of units known as base pairs. If the information were fragmented in a regular fashion—for example, if it were cut every ten thousand base pairs—there would be no way to identify each fragment’s immediate neighbors. It would be like owning a huge, multivolume novel without any numbering system: it would be almost impossible to determine with which book to start and which to proceed to next. Similarly, without some way of tracking the order of the genetic information, it would be impossible to assemble the sequence of each subfragment into the big continuum of the entire chromosome. The fragments are thus cut so that their ends overlap. With even a few hundred base pairs of overlap, the shared sequences at the end of the fragments can be used to determine the relative position of the different fragments. The different pieces can then be connected into one long unit, or sequence.

There are two common ways to fragment DNA, the basic unit of genetic information, to generate a library. The first is to disrupt the long strands of DNA by forcing them rapidly through a narrow hypodermic needle, creating forces that tear, or shear, the strands into short fragments. The advantage of this method is that the fragment ends are completely random. The disadvantage is that the sheared ends must be modified for easy joining, or ligation. The other method is to use restriction endonucleases, enzymes that recognize specific short stretches of DNA and cleave the DNA at specific positions. To create a library, scientists employ restriction enzymes that recognize four-base-pair sequences for cutting. Normally, the result of cleavage with such an enzyme would be fragments with an average size of 256 base pairs. If the amount of enzyme in the reaction is limited, however, only a limited number of sites will
be cut, and much longer fragments can be generated. The ends created by this cleavage are usable for direct ligation into vectors, but the distribution of cleavage sites is not as random as that produced by shearing.

In a conventional library, information is imprinted on paper pages that can be easily replicated by a printing press and easily bound into a complete unit such as a book. Genetic information is stored in the form of DNA. How can the pieces of a genome be stored in such a way that they can be easily replicated and maintained in identical units? The answer is to take the DNA fragments and attach, or ligate, them into lambda phage
DNA. When the phage infects bacteria, it makes copies of itself. If the genomic fragment is inserted into the phage DNA, then it will be replicated also, making multiple exact copies (or clones) of itself.

To make an actual library, DNA is isolated from an organism and fragmented as described. Each fragment is then randomly ligated into a lambda phage. The pool of lambda phage containing the inserts is then spread onto an agar plate coated with a “lawn” or confluent layer of bacteria. Wherever a phage lands, it begins to infect and kill bacteria, leaving a clear spot, or “plaque,” in the lawn. Each plaque contains millions of phages with millions of identical copies of one fragment from the original genome. If enough plaques are generated on the plate, each one containing some random piece of the genome, then the entire genome may be represented in the summation of the DNA present in all the plaques. Since the fragment generation is random, however, the completeness of the genomic library can only be estimated. It takes 800,000 plaques containing an average genomic fragment of 17,000 base pairs to give a 99-percent probability that the total will contain a specific human gene. While this may sound like a large number, it takes only fifteen teacup-sized agar plates to produce this many plaques. A genetic library pool of phage can be stored in a refrigerator and plated out onto agar petri dishes whenever needed.

How Can a Specific Gene Be Pulled Out of a Library?

Once the entire genome is spread out as a collection of plaques, it is necessary to isolate the one plaque containing the specific sequences desired from the large collection. To accomplish this, a dry filter paper is laid onto the agar dish covered with plaques. As the moisture from the plate wicks into the paper, it carries with it some of the phage. An ink-dipped needle is pushed through the filter at several spots on the edge, marking the same spot on the filter and the agar. These will serve as common reference points. The filter is treated with a strong base that releases the DNA from the phage and denatures it into single-stranded form. The base is neutralized, and the filter is incubated in a salt buffer containing radioactive single-stranded DNA. The radioactive DNA, or “probe,” is a short stretch of sequence from the gene to be isolated. If the full gene is present on the filter, the probe will hybridize with it and become attached to the filter. The filter is washed, removing all the radioactivity except where the probe has hybridized. The filters are exposed to film, and a dark spot develops
over the location of the positive plaque. The ink spots on the filter can then be used to align the spot on the filter with the positive plaque on the plate. The plaque can be purified, and the genomic DNA can then be isolated for further study.

It may turn out that the entire gene is not contained in the fragment isolated from one phage. Since the library was designed so that the ends of one fragment overlap with the adjacent fragment, the ends can be used as a probe to isolate neighboring fragments that contain the rest of the gene. This process of increasing the amount of the genome isolated is called genomic walking.

Key Terms



genome

:

all the genetic material carried by a cell




lambda (λ) phage

:

a virus that infects bacteria and then makes multiple copies of itself by taking over the infected bacterium’s cellular machinery




ligation

:

the joining together of two pieces of DNA using the enzyme ligase





Bibliography

Bird, R. Curtis, and Bruce F. Smith, eds. Genetic Library Construction and Screening: Advanced Techniques and Applications. New York: Springer, 2002. Print.

Bishop, Martin J., ed. Guide to Human Genome Computing. 2nd ed. San Diego: Academic, 1998. Print.

Cooper, Necia Grant, ed. The Human Genome Project: Deciphering the Blueprint of Heredity. Foreword by Paul Berg. Mill Valley: University Science, 1994. Print.

Dale, Jeremy, Malcolm von Schantz, and Nick Plant. “Genomic and cDNA Libraries.” From Genes to Genomes: Concepts and Applications of DNA Technology. 3rd ed. Chichester: Wiley, 2012. Print.

Danchin, Antoine. The Delphic Boat: What Genomes Tell Us. Trans. Alison Quayle. Cambridge: Harvard UP, 2002. Print.

Hoogenboom, H. R. “Designing and Optimizing Library Selection Strategies for Generating High-Affinity Antibodies.” Trends in Biotechnology 15.2 (1997): 62–70. Print.

Klug, William S., et al. Essentials of Genetics. 8th ed. Boston: Pearson, 2013. Print.

Primrose, S. B., and R. M. Twyman. “Genomic DNA Libraries Are Generated by Fragmenting the Genome and Cloning Overlapping Fragments in Vectors.” Principles of Gene Manipulation and Genomics. 7th ed. Malden: Blackwell, 2006. Print.

Sambrook, Joseph, and David W. Russell. Molecular Cloning: A Laboratory Manual. 4th ed. Cold Spring Harbor: Cold Spring Harbor Laboratory, 2012. Print.

Sandor, Suhai, ed. Theoretical and Computational Methods in Genome Research. New York: Plenum, 1997. Print.

Watson, James D., et al. Recombinant DNA: Genes and Genomes: A Short Course. 3rd ed. New York: Freeman, 2007. Print.

In To Kill a Mockingbird, how does Calpurnia fit into the social hierarchy in chapter three? Which characters have more power than she does?...

In chapter three of To Kill a Mockingbird, Calpurnia holds a significant amount of power in the Finch household. This chapter is set months before Aunt Alexandra comes to live with the family, so Calpurnia's word is law until that happens. Atticus sits at the top of the household hierarchy, Calpurnia comes in second, Jem is third, and of course, Scout is fourth. However, when Walter Cunningham comes to lunch on the first day of school, he sits higher than Scout on the hierarchy because he is a guest. Due to the code of hospitality, a guest's desires come before anyone who lives in the home. Therefore, when Walter asks for the syrup to drown his vegetables in, Calpurnia gives it to him. Scout is so shocked at Walter's behavior that she vocally questions him at the table. As a result, Calpurnia takes Scout into the kitchen and asserts her teaching authority by saying the following:

"Don't matter who they are, anybody sets foot in this house's  yo' comp'ny, and don't you let me  catch you remarkin' on their ways like you was so high and mighty! Yo' folks might be better'n the Cunninghams but it don't count for nothin' the way you're disgracin' e'em--if you can't act fit to eat at the table you can just set here and eat in the kitchen!" (24-25).

Not only does Calpurnia use her position as the Finch household motherly figure to teach Scout a lesson, but she brings up the Cunninghams and their social position in Maycomb as well. The Cunninghams are poor, white farmers, so they fall beneath the Finches socially, yet they are higher than Calpurnia because she is black. 

Another family that has more social power than Calpurnia is the Ewells. Scout meets her first Ewell in chapter three, and she learns that not only are they filthy, but they also have no manners, respect, or self-control. For example, Miss Caroline shrieks when she finds a louse in Burris' hair. Then she is mortified when Burris speaks to her disrespectfully as follows:

"Ain't no snot-nosed slut of a schoolteacher ever born c'n make me do nothing'! You ain't makin' me go nowhere, missus. You just remember that, you ain't makin' me go nowhere!" (28).

Burris gets away with talking to his teacher this way because he is part of the lowest social class in Maycomb. People just leave the Ewells alone because they are so unruly and unmanageable. The irony lies in the fact that Calpurnia is more educated (proven because she taught Scout to write) and more polite than any of the Ewells, but since she is black, she is treated as a second-class citizen even beneath the Ewells. 

Therefore, based on characters presented in chapter three, the social hierarchy would look something like this:

1. Atticus Finch, Jem, and Scout (financially stable, white landowner, professional, educated)

2. The Cunninghams (poor, white landowners)

3. Miss Caroline (educated and white)

4. The Ewells (poor, white and uneducated)

5. Calpurnia (educated, black)

As said before, Calpurnia has power and influence over Jem and Scout because she is supported by Atticus in the Finch household. For instance, when Scout attempts to get Calpurnia fired for sternly instructing her about manners during lunch, Atticus tells Scout the following:

"I've no intention of getting rid of her, now or ever. We couldn't operate a single day without Cal, have you ever thought of that? You think about how much Cal does for you, and you mind her, you hear?" (25).

Therefore, Calpurnia has power over Scout in the Finch home, but not so much in Maycomb where she doesn't have any social influence at all. Calpurnia's quality of life is better than that of the Cunninghams and Ewell's, though. She has a steady job and can live independently. However, socially, Calpurnia doesn't have much of a figurative leg to stand on because she is black. 

What are transient ischemic attacks (TIAs)?

Causes and Symptoms

A transient ischemic attack (TIA) is very similar to a stroke. Most physicians define a TIA as an episode of strokelike symptoms that fully resolves within twenty-four hours. A stroke, on the other hand, is defined as an episode that produces neurological symptoms that are permanent.

Strokes and TIAs are caused when the blood supply to the brain is interrupted. This interruption may occur because of a hemorrhage in an artery in the brain. Other causes of stroke or TIA may include a blood clot or piece of plaque that breaks loose from somewhere else in the body and eventually lodges in an artery that feeds the brain, or from severe narrowing in an artery that feeds the brain. Symptoms from a stroke or TIA that originates in the carotid arteries
(the main arteries in the front of the neck) include weakness or numbness on one side of the body, temporary loss of vision in one eye, and difficulty speaking. When the back of the brain is damaged, symptoms such as dizziness, difficulty walking, or a drop attack (sudden loss of leg strength) may occur.

One might think that since the symptoms of a TIA go away, such an attack is not a serious condition. However, a TIA is often a warning signal of an impending stroke. For this reason, anyone suffering a TIA should immediately seek medical attention.

The risk factors for TIA and stroke are similar. They include high blood pressure, high cholesterol, smoking, diabetes mellitus, advancing age, cardiac disease (especially irregular heart rhythm problems), stress, and lack of physical activity. Genetics can make one more likely to have a stroke or a TIA as well.

Treatment and Therapy

A person experiencing symptoms of a TIA should call paramedics in order to be seen in an emergency room immediately. Doctors can assess the patient’s situation and determine whether treatment can be initiated that will limit the amount of time that the brain is starved of oxygen. A stroke has been referred to as “brain attack” to underscore the need to seek prompt medical attention quickly, as one would for a heart attack.

Diagnostic tests will likely include magnetic resonance imaging (MRI) of the brain to check for hemorrhage or damage. Other tests may include magnetic resonance angiography (MRA) of the arteries or an ultrasound of the arteries that serve the brain. If these studies show a narrowing of the carotid arteries, then surgery can be done to remove the narrowed section before it causes more damage.

In some cases, medications will be used to lessen the risk of a full-blown stroke. They may include anticoagulants (blood thinners) and antiplatelet drugs such as aspirin, clopidogrel (Plavix), ticlopidine, and dipyridamole (Aggrenox). Drugs that lower cholesterol may also be prescribed.

Bibliography

Adams, Harold P., Jr., Vladimir Hachinski, and John W. Norris. Ischemic Cerebrovascular Disease. New York: Oxford University Press, 2001.

American Stroke Association. http://www.stroke association.org.

Chaturvedi, Seemant, and Steven R. Levine, eds. Transient Ischemic Attacks. Malden, Mass.: Blackwell Futura, 2004.

Kikuchi, H., ed. Strategic Medical Science Against Brain Attack. New York: Springer, 2002.

Parker, James N., and Philip M. Parker, eds. The Official Patient’s Sourcebook on Transient Ischemic Attack. Rev. ed. San Diego, Calif.: Icon Health, 2004.

"Transient Ischemic Attack (TIA)." Mayo Clinic, March 3, 2011.

"Transient Ischemic Attack (TIA)." National Stroke Association, 2013.

Wood, Debra. "Transient Ischemic Attack." Health Library, September 30, 2012.

What is typhus? |

Causes and Symptoms

The causative agent of epidemic
typhus is the bacterium Rickettsia prowazeckii, an obligate intracellular parasite. These bacteria are transmitted to humans following the bite from an infected body louse,
Pediculus humanus corporis. The pathogen is excreted with the louse feces and invades the site of a louse bite when the bitten host scratches the bite. The onset of the disease is marked by a high and prolonged fever with accompanying headache and rash. The bacteria are spread throughout the body through the bloodstream and can cause secondary lesions in many tissues, including the kidneys, heart, and brain. Mortality can be as high as 40 to 60 percent in untreated cases.

Treatment and Therapy

Antibiotic treatment is essential for reducing the severity of the disease, and chloramphenicol, tetracycline, and doxycycline are the antibiotics of choice. Improved sanitation and living conditions since the 1920s have virtually eliminated this disease in countries such as the United States. The last US epidemic was in 1922. Since then, there have been sporadic reports of isolated cases involving transmission from flying squirrels, indicating a possible animal reservoir; however, there is no real evidence to support this. Epidemic typhus still persists in some regions of Africa, Central America, and South America. The best course of action for prevention is to practice good hygiene and sanitation, and to avoid areas where there might be rat fleas and lice.

Perspective and Prospects

Epidemic typhus, also known as jail fever, is primarily a disease of crowded, substandard living conditions and poor sanitation. Millions of cases occurred in the trenches of World War I and in the concentration camps of World War II. Anne Frank, the noted teenage diarist, died of typhus contracted while at a concentration camp. It has been said that Napoleon’s retreat from Russia was started by a louse, and that lice have defeated the most powerful armies of Europe and Asia.

The pioneering investigations of Howard Taylor Ricketts
and Stanislas von Prowazeck in the early twentieth century paved the way for the discovery of both the bacteria and the louse vector, although both men died from the disease that they studied. They were honored posthumously when the bacterium was named Rickettsia prowazeckii.

Bibliography

Dugdale, David C. III, Jatin M. Vyas, and David Zieve. "Typhus." MedlinePlus, Oct. 6, 2012.

Eremeeva, Marina E., and Gregory A. Dasch. "Rickettsial (Spotted and Typhus Fevers) and Related Infections (Analplasmosis and Ehrlichiosis." Centers for Disease Control and Prevention, July 1, 2011.

Lock, Stephen, John Last, and George M. Dunea, eds. The Oxford Companion to Medicine. 3d ed. New York: Oxford University Press, 2006.

Murray, Patrick R., Ken S. Rosenthal, and Michael A. Pfaller. Medical Microbiology. 7th ed. Philadelphia: Mosby/Elsevier, 2013.

Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: An Introduction. 11th ed. San Francisco: Pearson Benjamin Cummings, 2013.

"Typhus Fever (Endemic Louse-Borne Typhus)." World Health Organization, 2013.

Zinsser, Hans. Rats, Lice, and History. New York: Black Dog & Leventhal, 1996.

What is collagen? |

Structure and Functions

Collagen is a complex protein made up of three separate polypeptide chains that form a triple helix. These polypeptides are unusual because every third amino acid is a glycine and because prolines make up an additional 17 percent of the chains. There are at least twenty-eight types of collagen made up of forty-three distinct polypeptide chains, each coded for by a different gene. For example, type I collagen, the most common type, has two chains classified as alpha-1 and alpha-2. These peptides are initially produced on the rough endoplasmic reticulum
(ER) and then processed in the ER lumen, where sequences at the ends are removed and hydroxyl groups are added to many of the chains’ prolines and lysines. The triple helix then formed is called procollagen. Further processing, including preparation for secretion, takes place in the Golgi bodies. Once secreted, more end sequences are cleaved off to form collagen (also called tropocollagen). In the extracellular region, collagen molecules associate into collagen fibrils and eventually collagen fibers.

Collagen is a flexible but not stretchable protein that is an important component of most connective tissues. It is the primary component of tendons and ligaments, giving them the requisite strength to connect muscles to bones and bones to other bones or organs. Cartilage found at joints and in many other structures is mostly collagen. The connective tissues found in the dermal layer of the skin, the capsules surrounding internal organs, and blood vessels are also primarily made of collagen. Bones are initially formed from collagen, which then serves as a matrix for calcium phosphate deposition. (Collagen fragments have even been extracted from fossilized dinosaur bones.) During healing, excess collagen production can lead to scar tissue formation. Collagen can be heat-treated to produce gelatin or animal-based glues, and injected collagen is often used in cosmetic procedures to plump lips or smooth out wrinkles.

Disorders and Diseases

Collagen is associated with many disorders. Osteogenesis imperfecta (brittle bone disease) is caused by mutations in the gene for the alpha-1 protein in type I collagen. An inherited form of osteoporosis is caused by a defect in the same gene. Ehlers-Danlos syndrome, which results in hyperextensible joints and fragile, stretchable skin, is caused by defects in types III and V collagen. A form of early-onset osteoarthritis is caused by a lack of functional type VI collagen, and in all forms of osteoarthritis
cartilage is lost from the ends of bones at joints. In rheumatoid arthritis, modification of type II collagen forms new antigens that are attacked by the immune system. Vitamin C deficiency decreases activity of the enzymes that add hydroxyl groups to proline, thus leading to lowered amounts of functional type I collagen, which causes
scurvy.

Bibliography

Abreu-Velez, Ana Maria, and Michael S. Howard. "Collagen IV in Normal Skin and in Pathological Processes." North American Journal of Medical Sciences 4, no. 1 (2012): 1–8.

"Collagen Vascular Disease." Medline Plus, February 9, 2011.

Fratzl, Peter. Collagen: Structure and Mechanics. New York: Springer, 2008.

Myllyharju, Joahanna, and Kari Kivirkko. “Collagen and Collagen-Related Diseases.” Annals of Medicine 33 (2001): 7–21.

"Questions and Answers about Heritable Disorders of Connective Tissue." National Institute of Arthritis and Musculoskeletal and Skin Diseases, October 2011.

"Types of OI." Osteogenesis Imperfecta Foundation, 2012.

Whitford, David. Proteins: Structure and Function. Hoboken, N.J.: John Wiley & Sons, 2005.