What is punctuated equilibrium? |

Evolutionary Patterns

Nineteenth century English naturalist Charles Darwin
viewed the development of new species as occurring slowly by a shift of characteristics within populations, so that a gradual transition from one species to another took place. This is now generally referred to as phyletic gradualism. A number of examples from the fossil record
were put forward to support this view, particularly that of the horse, in which changes to the feet, jaws, and teeth seem to have progressed in one direction over a long period of time. Peter Sheldon in 1987 documented gradual change in eight lineages of trilobites over a three-million-year period in the Ordovician period of Wales. Despite these and other examples (some of which have been reinterpreted), it is clear that the fossil record more commonly shows a picture of populations that are stable through time but are separated by abrupt morphological breaks. This pattern was recognized by Darwin but was attributed by him to the sketchy and incomplete nature of the fossil record. So few animals become fossilized, and conditions for fossilization are so rare, that he felt only a fragmentary sampling of gradual transitions was present, giving the appearance of abrupt change.

One hundred years later, the incompleteness of the fossil record no longer seemed convincing as an explanation. In 1972, Niles Eldredge and Stephen Jay Gould
published their theory of the evolutionary process, which they called “punctuated equilibrium.” This model explains the lack of intermediates by suggesting that evolutionary change occurs only in short-lived bursts in which a new species arises abruptly from a parent species, often with relatively large morphological changes, and thereafter remains more or less stable until its extinction.

The Process of Punctuated Equilibrium

A number of explanations have been put forward to show how this process might take place. One of these, termed allopatric speciation,
was first proposed by Ernst Mayr in 1963. He pointed out that a reproductive isolating mechanism is needed to provide a barrier to gene flow and that this could be provided by geographic isolation. Allopatric or geographical isolation could result when the normal range of a population of organisms is reduced or fragmented. Parts of the population become separated in peripheral isolates, and if the population is small, it may become modified rapidly by natural selection or genetic drift, particularly if it is adapting to a new environment. This type of process is commonly called the founder effect, because it is the
characteristics of the small group of individuals that will overwhelmingly determine the possible characteristics of their descendants. As the initial members of the peripheral isolate may be few in number, it might take only a few generations for the population to have changed enough to become reproductively isolated from the parent population. In the fossil record, this will be seen as a period of stasis representing the parent population, followed by a rapid morphological change as the peripheral population is isolated from it and then replaces it, either competitively or because it has become extinct or has moved to follow a shifting habitat. Because this is thought to take place rapidly in small populations, fossilization potential is low, and unequivocal examples are not common in the fossil record. However, in 1981, Peter Williamson published a well-documented example from the Tertiary period of Lake Turkana in Kenya, which showed episodes of stasis and rapid change in populations of freshwater
mollusks. The increases in evolutionary rate were apparently driven by severe environmental change that caused parts of the lake to dry up.

Punctuated changes may also have taken place because of heterochrony, which is a change in the rate of development or timing of appearance of ancestral characters. Paedomorphosis, for example, would result in the retention of juvenile characters in the adult, while its opposite, peramorphosis, would result in an adult morphologically more advanced than its ancestor. Rates of development could be affected by a mutation, perhaps resulting in the descendant growing for much longer than the ancestral form, thus producing a giant version. These changes would be essentially instantaneous and thus would show as abrupt changes of species in the fossil record.

Impact and Applications

The publication of the idea of punctuated equilibrium ignited a storm of controversy that still persists. It predicts that speciation can be very rapid, but more important, it is consistent with the prevalence of stasis over long periods of time so often observed in the fossil record. Species had long been viewed as flexible and responsive to the environment, but fossil species showed no change over long periods despite a changing environment. Biologists have thus had to review their ideas about the concept of species and the processes that operate on them. Species are now seen as real entities that have characteristics that are more than the sum of their component populations. Thus the tendency of a group to evolve rapidly or slowly may be intrinsic to the group as a whole and not dependent on the individuals that compose it. This debate has helped show that the fossil record can be important in detecting phenomena that are too large in scale for biologists to observe.

Key terms



allopatric speciation

:

a theory that suggests that small parts of a population may become genetically isolated and develop differences that would lead to the development of a new species





heterochrony


:

a change in the timing or rate of development of characters in an organism relative to those same events in its evolutionary ancestors




phyletic gradualism

:

the idea that evolutionary change proceeds by a progression of tiny changes, adding up to produce new species over immense periods of time





Bibliography

Ayala, Francisco J. “Punctuated Equilibrium and Species Selection.” Back to Darwin: A Richer Account of Evolution. Ed. John B. Cobb Jr. Grand Rapids: Eerdmans, 2008. Print.

Chevin, Luis-Miguel. "Genetic Constraints on Adaptation to a Changing Environment." Evolution 67.3 (2013): 708–721. Print.

Eldredge, Niles. Time Frames: The Rethinking of Darwinian Evolution and the Theory of Punctuated Equilibria. New York: Simon, 1985. Print.

Eldredge, Niles, and Stephen Jay Gould. “Punctuated Equilibria: An Alternative to Phyletic Gradualism.” Models in Paleobiology. Ed. Thomas J. M. Schopf. San Francisco: Freeman, 1972. Print.

Gould, Stephen Jay. “The Meaning of Punctuated Equilibria and Its Role in Validating a Hierarchical Approach to Macroevolution.” Perspectives on Evolution. Ed. Roger Milkman. Sunderland: Sinauer, 1982. Print.

Gould, Stephen Jay, and Niles Eldredge. “Punctuated Equilibrium: The Tempo and Mode of Evolution Reconsidered.” Paleobiology 3 (1977): 115–151. Print.

Kulathinal, Rob J., Jianping Xu, and Rama S. Singh. Rapidly Evolving Genes and Genetic Systems. Oxford: Oxford UP, 2012. Digital file.

Pennell, Matthew W., Luke J. Harmon, and Josef C. Uyeda. "Is There Room for Punctuated Equilibrium in Macroevolution?" Trends in Ecology & Evolution 29.1 (2014): 23–32. Print.

Prothero, Donald R. Bringing Fossils to Life: An Introduction to Paleobiology. 3d ed. New York: Columbia UP, 2013. Print.

Sepkoski, David, and Michael Ruse, eds. The Paleobiological Revolution: Essays on the Growth of Modern Paleontology. Chicago: U of Chicago P, 2009. Print.

Somit, Albert, and Steven A. Peterson, eds. The Dynamics of Evolution: The Punctuated Equilibrium Debate in the Natural and Social Sciences. Ithaca: Cornell UP, 1992. Print.

Compare the passage below to Orgon's description of Tartuffe in Act 1.5, II. 30-40. What does this say about Tartuffe's piety? Matthew 6:6 ...

Tartuffeis a play about religious hypocrisy. In the play, Orgon and Madame Pernelle are fooled by Tartuffe. They believe him to be holy and righteous. The audience, however, is aware from the beginning that Tartuffe is a fraud. In the scene you are asking about, Orgon describes his first encounter with Tartuffe. He says, “Every day he came to church and knelt/And from his groans, I knew just what he felt” (32-33). Tartuffe is...

Tartuffe is a play about religious hypocrisy. In the play, Orgon and Madame Pernelle are fooled by Tartuffe. They believe him to be holy and righteous. The audience, however, is aware from the beginning that Tartuffe is a fraud. In the scene you are asking about, Orgon describes his first encounter with Tartuffe. He says, “Every day he came to church and knelt/And from his groans, I knew just what he felt” (32-33). Tartuffe is overt and loud in his worship. According to the Bible verse above, one should worship privately (“enter into thy closet…pray to thy father in secret”). Tartuffe wants people to pay attention to him: “His fervent prayers to heaven and deep sighs/Made them witness his deep spiritual pain” (39-40). The Bible verse, on the other hand, suggests that God will reward prayers given to him in secret. Cleante reiterates this in his discussion with Orgon, telling him that loud prayers are not necessarily the sign of a holy man. “Religious passion worn as a façade/Abuses what’s sacred and mocks God (128-129). Orgon cannot see past Tartuffe’s seeming religious zeal to the man underneath, but the rest of the family has no problem identifying his religious hypocrisy.

Analyze in detail the collapses of Rome (200-600 CE).

Before I answer this, I do want to offer a caveat. The decline of the Roman empire is a subject that has been the cause of some historiographical controversy — historians themselves do not agree about the correct methods and ways to analyze and explain the decline of the Roman empire. What I offer is a received account although it is not the only account that exists. (There are dozens, if not scores, more!) Some even question if Rome fell; however, since your question assumes that it did, indeed, decline, we'll take that as our starting point. 

You also ask about the collapses of Rome until 600 CE. I'm not sure whether the plural is a typo or whether you're referring to multiple collapses. If it's the latter, I address that at the very end.

Also, the standard date for the 'fall' of Rome is 476 CE when the German prince Odovacar deposed the last of the Roman emperors, Romulus Augustulus. From that date onwards the Roman empire effectively ceased to exist except as a collection of many kingdoms and fiefdoms (many of which fought against one another rendering the former Roman empire a battleground of sorts, something which probably only served to usher in the so-called 'Dark Ages' even faster).

The only way to take ca 600 CE as the date of the collapse is to regard Justinian I, the Byzantine emperor who constructer the Hagia Sophia, as the last of the Romans. There is some credence to this. Although he was part of the 'Roman east,' he did attempt to regain some of the 'Roman west'. His generals even successfully battled the Ostrogoths and the Vandals. However, it would be inaccurate to consider his successors to be part of 'Rome'. Especially since the Byzantine empire flourished for almost a thousand years after western Rome fell.

According to the 18th century historian, Edward Gibbon, Rome fell because of persistent invasion from barbarians. Gibbon felt that the adoption of Christianity had somehow 'emasculated' Rome and left it open to more 'virile' conquerers — indeed, the period between 200 CE and 600 CE was marked by incursions from the Ostrogoths, Visigoths, Huns, and Vandals. This was undoubtedly destabilizing for Rome and was one of the contributing factors for its decline. However, it's not at all obvious that Christianity was responsible for this. Gibbon's explanation also ignores other important factors.

One extremely significant event was the battle of Hadrianople in 378 CE. At this battle,  the emperor Valens and around 10000 of his soldiers were killed in a single day by the Goths. This allowed the gradual invasion of Rome by external forces and culminated in the deposition of Romulus Augustulus. 

All the warfare, combined with natural disasters such as a plague, had also decimated Rome's population and consequently left it weakened.

Around 300 CE and following, there was also a great economic depression because of problems with the slave trade. Rome may have had superior agricultural technology, but in the absence of labor to take care of this technology, it just felt to disuse, which only aided the economic depression.

Oppressive taxation also crippled Rome and undoubtedly let to its decline.

All of these factors can be tied into the growth of a corrupt political system.

So, repeated invasions and the decline in population that went with it, as well as natural disasters, economic depression, and corrupt politics all eventually led to the collapse of Rome.

Now, if you think that there were collapses, perhaps you're referring to various conquests of the city by invading forces — it was the Visigoths in 410 CE and the Vandals in 455 CE. 

This is too complex a topic for a short answer to do it full justice. That's why there are several books on the subject! Here are two recent ones:

Ward-Perkins, Bryan (2005) The Fall of Rome and the End of Civilisation. Oxford University Press.

Heather, Peter (2005) The Fall of the Roman Empire. Macmillan.

What is a macrobiotic diet?

Overview

Japanese philosopher George Ohsawa developed the macrobiotic
lifestyle, which includes the macrobiotic diet, meditation,
exercise, and stress reduction. The lifestyle also involves limiting exposure to
pesticides. Ohsawa also believed that eating healthy food is part of a process
that promotes world peace and harmony.

The macrobiotic diet is based on the traditional Japanese diet. Food choices
for the diet are based on the principle of yin and yang,
opposing forces that are viewed as needing to balance each other. In the 1960s,
Ohsawa’s student Michael Kushi, of the Kushi Institute, popularized the
macrobiotic diet in the United States. The original diet proposed by Ohsawa is now
viewed by macrobiotic diet teachers to be too restrictive; the current macrobiotic
diet has been modified to prevent problems such as scurvy, other
forms of malnutrition, and death, which were reported in some followers of the
original diet.

Organic foods that are minimally processed are recommended for the macrobiotic diet. Up to 60 percent of the diet’s components are whole grains and up to 30 percent are vegetables, with the remainder of the diet being made up of beans and seaweed. The diet does not include meat, animal fats, dairy, eggs, refined sugar, or artificial sweeteners. Warm drinks are to be avoided too.

The diet also recommends specific approaches to food preparation. For example, only gas stoves are to be used, and cooking vessels or utensils containing copper, aluminum, or Teflon are to be avoided.

Mechanism of Action

As a means of restoring the balance of yin and yang, teachers of macrobiotics attempt to adjust the individual person’s diet based on the areas affected by illness.

Uses and Applications

Proponents of the macrobiotic diet state that it can have curative properties for cancer and acquired immunodeficiency syndrome (AIDS), can prevent heart disease, and can contribute to an overall sense of well-being.

Scientific Evidence

No randomized-controlled clinical trials of the macrobiotic diet exist. Reports of macrobiotic dieters who have recovered from cancer are anecdotal.

Safety Issues

The macrobiotic dieter may become deficient in vitamins B12 or D,
fluid, calcium, iron, and riboflavin. Experts recommend that pregnant or nursing
women and children on the macrobiotic diet may need to consume eggs, dairy
products, or other forms of supplementation to prevent nutritional deficiencies
that can lead to rickets, retarded growth, or slow motor or mental
development in the fetus.

Bibliography

American Cancer Society. “Macrobiotic Diet.” Available at http://www.cancer.org/treatment.

Kushi Institute. “What Is Macrobiotics?” Available at http://www.kushiinstitute.org/html/what_is_macro.html.

MD Anderson Cancer Center, University of Texas. “Macrobiotics: Detailed Scientific Review.” Available at http://www.mdanderson.org/education-and-research.

What are the healing properties of humor?

Overview

The Old Testament references the healing properties of humor: “A merry heart doeth good like a medicine.” Throughout the centuries, court jesters have been hired by monarchs to relieve the stress of governmental duties. As early as the thirteenth century, surgeons used humor to distract patients from pain.

In modern times, a systematic approach appears to be developing, consisting of exposure to true mirthful laughter in a supportive environment, under the guidance of a qualified leader or therapist, and combined with attitudinal healing and conventional medicine.

Mechanism of Action

Laughter is thought to trigger the release of endorphins, the body’s natural painkillers. Laughter relaxes muscles, which may then also reduce four neuroendocrine hormones associated with the stress response: epinephrine, cortisol, dopac, and growth hormone.

Laughter moves lymph fluid around the body because of the convulsions that come from the process of laughing. This process helps clear waste products from organs and tissues and boosts the immune system. Laughter is also thought to boost the immune system by increasing both salivary immunoglobulin (IgA) and blood levels of IgA, along with IgM and IgG, a substance called complement 3, which helps antibodies destroy infected cells. Laughter boosts the immune system also by helping the body increase the number and activity of natural killer cells, the number and level of activation of helper T cells, and the ratio of helper to suppressor T cells. Laughter also is thought to increase levels of gamma interferon, a complex substance that plays an important role in the maturation of B cells, the growth of cytotoxic T cells, and the activation of natural killer cells.

Finally, laughter appears to cause the tissue that forms the inner lining of blood vessels, the endothelium, to dilate or expand to increase blood flow.

Uses and Applications

Researchers have described different types of humor. Passive humor is created through entertainment, such as watching a film or reading a book. Humor production involves finding humor in stressful situations.

Hospitals and ambulatory care centers have incorporated spaces where humorous
materials can be accessed, and they often have clowns and comedians perform or
interact with patients to help make them laugh. Other hospitals create what are
called laughter clubs or use volunteer groups to visit hospitalized persons to
provide laughter. Another type of laughter therapy is laughter yoga.

Scientific Evidence

No double-blind studies have been conducted on laughter therapy, but many
observational studies exist. The most well-known record of the benefits of
laughter and humor healing is the book Anatomy of an Illness as Perceived
by the Patient by Norman Cousins. In 1964, Cousins was
diagnosed with a debilitating inflammatory condition. He experimented with
laughter (among other complementary therapies) by systematically watching the
television show Candid Camera, by watching Marx Brothers
films, and by reading humorous books. He wrote “I made the joyous discovery that
ten minutes of genuine belly laughter had an anesthetic effect and would give me
at least two hours of pain-free sleep.”

The first study to prove that laughter helps heart health was performed by researchers at the University of Maryland and published in 2000. In this study, persons with heart disease were 40 percent less likely to laugh in a variety of situations, compared with people of the same age without heart disease. In the study, researchers compared the humor responses of three hundred people, one-half of whom either had suffered a heart attack or had undergone coronary artery bypass surgery. The other one-half were healthy, age-matched participants who did not have heart disease.

In another study at the University of Maryland (2005), some patients were shown disturbing films and others were shown humorous films. The funny films enhanced blood vessel health.

In a five-year study of persons with leg ulcers, researchers at the University of Leeds’ School of Healthcare showed that laughing gets the diaphragm moving, playing a vital part in moving blood around the body. In a separate study by Loma Linda University in Southern California, researchers studied men and women taking medication for diabetes, high blood pressure, and high cholesterol and proved that those prescribed mirthful laughter in the form of thirty minutes of comedy every day showed considerable reduction in stress hormone levels.

Choosing a Practitioner

Usually a person does not choose a single practitioner but is placed in a group when already being treated at an institution. It also is plausible that a person could self-treat.

Safety Issues

Laughter therapy is cost-effective and noninvasive.

Bibliography

Bennett, Paul N, et al. “Laughter and Humor Therapy in Dialysis.” Seminars in Dialysis 27.5 (2014): 488–493. MEDLINE Complete. Web. 27 Jan. 2016.

“Laughter Therapy.” Cancer Treatment Centers of America. Rising Tide, 2015. Web. 27 Jan. 2016.

Cousins, Norman. Head First: The Biology of Hope and the Healing Power of the Human Spirit. New York: Penguin Books, 1989. Print.

Han, Byong-Hyon. Therapy of Social Medicine. Singapore: Springer, 2016. eBook Collection (EBSCOhost). Web. 27 Jan. 2016.

Stewart, Susan M. “Laughter: Nature’s Healing Refrain.” Healing with Art and Soul: Engaging One’s Self Through Art Modalities. Ed. Kathy Luethje. Newcastle upon Tyne: Cambridge Scholars, 2009. Print.

What is tetanus? |

Causes and Symptoms

Tetanus is a disease of the nervous system caused by the bacterium Clostridium tetani (C. tetani). Humans and most species of warm-blooded animals are susceptible to tetanus. This disease is not contagious, meaning it cannot be transmitted from one individual to another. It results from the contamination of a natural or surgical wound by spores (endospores) of C. tetani. The
bacteria grow in the wound and produce a toxin that spreads throughout the body and causes the symptoms of the disease. Neonatal tetanus is the appearance of tetanus in a child less than one month old; it is usually contracted by the infant directly following birth.

C. tetani is an anaerobic, endospore-forming bacterium. Anaerobic bacteria can grow only in an oxygen-free environment. In harsh environments or at times when oxygen is present, all species of Clostridia have the unique ability to form dormant (nongrowing) structures called endospores. These structures develop inside the bacterial cell and serve to protect the genetic material of the cell from harsh environmental stresses that would destroy an actively growing cell. Endospores are very resistant to disinfectants and temperature changes; thus, the bacteria can remain dormant until the surrounding environment becomes better suited for growth. C. tetani spores are found throughout the world in soil, human and animal intestines, and especially in soil fertilized with human or animal feces.

A person can get tetanus only if spores from the soil or elsewhere in the environment enter that person under the proper conditions to become living, growing bacteria. The bacteria will grow only if they enter a wound that is free from oxygen, such as a deep puncture wound or a wound that has considerable dead or crushed tissue. There are always a few cases of tetanus, however, that follow no apparent injury. Typical causes of
wounds that could be susceptible to tetanus are compound fractures; gunshots; dog bites; punctures caused by glass, thorns, needles, splinters, or rusty nails; “skin popping” by drug addicts; bedsores; outer ear infections; and dental extractions. The most feared form of tetanus, neonatal tetanus, is usually caused by the cutting of the
umbilical cord with an unsterile instrument or by improper care of the umbilical stump. In the United States, most cases of neonatal tetanus are found in home deliveries not attended by a health professional.

Spores of C. tetani enter the body through a wound or abrasion. In the absence of oxygen, they will germinate (revert from the dormant endospore state to become living, growing cells). The bacteria will grow and multiply but not spread from the initial site of infection. In many cases, the wound hardly appears to be infected at all. As it grows, C. tetani produces a toxin called tetanospasmin that can filter through the body. Once the toxin reaches the central nervous system, it binds to nerve cells, causing the beginning stages of symptoms to be seen. Symptoms can appear from one day to several months after infection, with the average incubation period (the time during which symptoms appear after infection) being three to twenty-one days. The wide range of incubation time depends on the amount of time needed for anaerobic conditions to develop and the time required for the toxin to reach the central nervous system.

The tetanus toxin, tetanospasmin, is a simple protein. No one knows why C. tetani makes this protein. It has no apparent role in the life of the bacterium, and it is unknown whether this toxin gives the bacterium any selective advantage for survival in the environment. It is unlikely that the bacterium makes this toxin merely to kill people and animals, yet the fact that it does kill them is all that is known about the toxin. Animals vary in their susceptibility to the effects of tetanospasmin; humans and horses are the most susceptible, while birds and cold-blooded animals are resistant. Tetanospasmin is the second most dangerous known toxin, and it is so powerful that an amount of toxin the size of one period on this page could kill thirty people. One milligram of toxin could kill 200 million laboratory mice.

To understand how tetanospasmin works to cause the symptoms of tetanus, one must first understand how muscles function. Most muscles in the body occur in pairs; one muscle in the pair, when contracted, causes that part of the body to move in one direction, and the opposing muscle in the pair, when contracted, causes that part of the body to move in the opposite direction. Normally, the nerves that control the muscle pairs stimulate one muscle in a pair to contract and signal the opposing muscle to relax. In this way, that part of the body is able to move. For example, in using an arm to lift an object, the nerves send a signal to the muscle in the front of the arm to contract and at the same time send a signal to the back of the arm to relax, so that the arm can bend upward at the elbow and lift the object. If the nerves did not signal the opposing muscle to relax, the contraction of the first muscle would cause the opposing muscle to stretch and trigger the “stretch reflex” in that muscle, causing that muscle to contract and counteract the stretch. Tetanus toxin works by binding to the nerve cells at nerve-muscle junctions and somehow
blocking the signal of relaxation to the opposing muscle; therefore, when one muscle in a pair of muscles contracts, both muscles contract. The final effect is called spastic paralysis, in which the muscles are in a state of continuous contraction, pulling against each other, causing rigidity in a normally movable part of the body.

The initial symptoms of tetanus include restlessness, irritability, a stiff neck, and difficulty swallowing. In about half of all cases, the initial symptoms include stiffness or spasms of the jaw muscles, known as lockjaw. Gradually, the skeletal muscles (muscles of the arms, legs, back, and stomach) become involved. Muscles move through stages of contractions, from merely twitching to rigid spasms that are brief but may be frequent, painful, and exhausting. Severe stages of the disease are characterized by tetanic spasms (sustained contractions) of some or all of the muscle groups. The slightest disturbance of the victim may cause spasms, generalized
seizures, or both. A typical tetanic seizure is characterized by a sudden burst of tetanic spasm of all muscle groups, causing clenching of the jaw to produce a grimace, arching of the back with the neck back, flexion of arms, clenching of fists on the chest, and extension of the lower extremities. The patient is completely conscious during such episodes and experiences intense pain. Some spasms may be severe enough to cause bones to break. Eventually, the muscles of the cardiac and respiratory systems can be affected. Spasms of the throat muscles and respiratory muscles may lead to suffocation or respiratory arrest. The toxin may affect the circulatory system and heart in such a way as to increase the heart rate, increase blood pressure, and cause constriction of blood vessels. Death caused by tetanus is usually a result of circulatory collapse or respiratory failure.

Treatment and Therapy

Tetanus is diagnosed mainly on the basis of the symptoms present and the case history of the patient—the vaccination record and the type of injury sustained. A patient with no recent history of tetanus vaccination who receives a puncture or trauma wound is often treated for tetanus with an injection of antitoxin even before any symptoms appear. Antitoxin is quite effective when given to prevent the symptoms from appearing, but less so when given after the symptoms have already appeared. While other diseases are diagnosed after the organism that causes the disease is isolated from the site of the infection, it is very difficult to diagnose tetanus based on the ability to isolate the C. tetani bacteria from the wound, for several reasons. First, Clostridia are present in almost every wound, but they do not always cause disease, so finding them does not necessarily mean that the bacteria are active. Second, there are many other contaminating bacteria
in wounds, which makes it difficult to tell which may be causing disease or whether Clostridia are there at all. In addition, the number of C. tetani bacteria needed to cause disease is quite small, which makes them harder to isolate. Finally, Clostridia, because of their anaerobic nature, are difficult to grow.

Tetanus may take from a few days to several weeks to run its course. Patients who exhibit certain patterns in the course of the disease usually have a poor chance of recovery. These include patients with a short incubation period between the time of the injury and the onset of seizures, patients who exhibit a rapid development from mild muscle spasms to tetanic spasms, patients with injuries close to the head, patients with a high frequency or strong severity of seizures, and patients who are very young or very old. Patients who do recover usually return to a completely normal state after a variable period of stiffness; except for possible damage to the lungs from pulmonary complications or bone fractures, tetanus leaves no permanent damage. Unfortunately, recovery from the disease does not make the patient immune to future attacks, as with other diseases. The amount of toxin needed to kill a person is not even close to enough toxin to stimulate the patient’s immune response to make the patient immune to the disease. Only vaccination with a large dose of inactive toxin can
give a person immunity to tetanus.

Tetanus is difficult to treat because no one knows exactly what the toxin does. Doctors know only what kinds of symptoms the toxin causes, so the treatment is mainly symptomatic and is directed at preventing the production of more toxin. Antitoxin is given to block the attachment to the nerve cells of any free toxin that might be circulating in the body. Antitoxin has absolutely no effect on toxin that is already fixed to nerve tissue, but it can fully neutralize any free toxin. Originally, doctors used serum from immunized horses as a source of antitoxin, but this caused serious side effects (namely, serum sickness) in patients, so it is recommended that only pooled hyperimmune human globin (purified serum from immunized humans) be used as a source of antitoxin. Second, large doses of an antibiotic such as penicillin are given to kill any remaining bacteria, in order to prevent the bacteria from producing more toxin. If the patient is allergic to penicillin, tetracycline or clindamycin can be given instead. In addition, the wound may need to be cleansed of any dead tissue, to remove the anaerobic environment necessary for growth of the bacteria.
Third, the muscle spasms need to be controlled. Mild muscle spasms are controlled with barbiturates and diazepam (Valium); severe spasms need a curarelike agent (D tubocurarine is used to poison the paralyzed muscles so that they do not contract) that completely paralyzes the patient. These various muscle relaxants are used to ease the contractions until the toxin already present at the nerve sites wears out. The patient can be put on a positive-pressure breathing apparatus to maintain respiration. A
tracheostomy (an operation in which an opening into the trachea, or windpipe, is made) may be necessary to minimize respiratory complications. Also, patients are often kept in quiet dark rooms that reduce auditory and visual stimuli, in order to minimize the frequency and severity of the tetanic spasms. Even with all these treatment measures, three out of five persons who contract tetanus will die.

The best means of controlling tetanus is prevention. In fact, tetanus is nearly 100 percent preventable with active or passive immunization. Active immunization involves stimulating a person’s immune system to produce its own antibody to fight off the disease. An injection of tetanus toxoid is given to immunize actively against tetanus. Tetanus toxoid is purified tetanus toxin that has been treated with formaldehyde to be rendered nontoxic (meaning that it will not cause any symptoms of tetanus) but is still capable of stimulating the immune system to produce antitoxin antibody. Active immunization usually lasts a long time, because the cells that make the antibody can keep making more antibody when the first batch runs out or whenever the person comes in contact with tetanus toxin in the future. The tetanus toxoid is usually administered as part of the DPT vaccine. This vaccine protects
against diphtheria (D), pertussis (P), and tetanus (T). In the United States, it is recommended that persons be immunized against tetanus at two, four, six, and eighteen months of age, with a booster at four to six years of age and one every ten years after that. Surveys indicate, however, that more than 50 percent of adults over sixty years of age are not protected against tetanus. It is as dangerous to receive too many booster shots for tetanus as it is to receive too few. With too few shots, a person runs the risk of succumbing to the disease and dying. With too many shots, a person runs the risk of developing a potentially fatal allergic reaction to the vaccine. It is best to keep careful records of all vaccinations and to be certain that one receives a tetanus booster every ten years.

Passive immunization involves giving a person antibodies (made in an outside source) that will protect that person from a disease, instead of stimulating the individual to make antibodies. Patients thought to be at risk for tetanus can be given an injection of antitoxin for protection. This type of protection works only for a short period of time, because once the antibody in the injection is used up, the patient cannot make more. The way to immunize infants passively against neonatal tetanus is to immunize their mothers actively. A pregnant patient immunized with tetanus toxoid will produce antitoxin that is passed on to the baby’s blood through the placenta. The baby is then born carrying some antitoxin antibodies in its blood that can protect it from neonatal tetanus.

Perspective and Prospects

As early as the fourth century BCE, Hippocrates described tetanus as a common killer of women in childbirth, wounded soldiers, and infants. It was not until 1889, however, that the cause of tetanus, C. tetani, was first isolated by Shibasaburo Kitasato. In the early twentieth century, W. T. Glenny and Gaston Ramon paved the way for the development of a tetanus vaccine by discovering tetanus toxoid. War-related cases of tetanus were virtually eliminated by vaccinating soldiers. During World War II, only 12 cases of tetanus were recorded among 2,735,000 hospital admissions for wounds and injuries in soldiers previously immunized. This result led most state legislatures in America to pass laws requiring adequate immunization for tetanus before entering school.

Despite advances in treatment, the mortality rate for tetanus is quite high. The United States has about one hundred cases per year, mostly in the very young, who are in frequent contact with the soil, or in the very old, who have weakened immune systems. Many cases in the United States arise from trivial but fairly deep injuries that are thought to be too minor to bring to a physician. Sporadic cases are most frequently seen in the South, the Southeast, and the Midwest.

Tetanus is relatively rare in developed countries, where routine immunizations are available; it is, however, a common and uncontrolled disease in the developing world. Tetanus is a health problem in developing countries because of the lack of immunization, unsanitary living conditions, and the performance of common wound-causing procedures (such as ear piercing, tattooing, circumcision, and abortion) in an unsanitary manner. Neonatal tetanus is often caused by mothers or midwives who cut the umbilical cord with an unsanitary instrument. In addition, it is a tradition in many developing nations to apply soil, clay, or cow dung to the cut umbilical cord, which can inoculate tetanus spores right into the wound. Throughout the world, nearly 3.5 million children (mostly under five years of age) die yearly of three infectious diseases for which immunization is available. Two million die of measles, eight hundred thousand die of tetanus, and six hundred thousand die of whooping cough; another four million die of various kinds of diarrhea. In parts of some developing nations, 10 percent of deaths within a month of birth are caused by neonatal tetanus. The
World Health Organization is making a concerted effort to reduce the incidence of tetanus—especially neonatal tetanus—in developing nations by providing the personnel and resources needed for vaccination. Strategies for reducing the incidence of neonatal tetanus include providing passive immunity to newborns through the immunization of the mothers. Also important are promotion of safe practices, such as clean deliveries and clean cord cutting, and ensuring that unsanitary substances are not applied to cord wounds.

Bibliography:

“CDC Report Finds Tetanus Reaching Younger Adults.” Vaccine Weekly, July 16, 2003, 21–22.

Hollenstein, Jenna. "Tetanus." Health Library, November 26, 2012.

Joklik, Wolfgang K., et al. Zinsser Microbiology. 20th ed. Norwalk, Conn.: Appleton and Lange, 1997.

Pan American Health Organization. World Health Organization. Control of Diphtheria, Pertussis, Tetanus, “Haemophilus influenzae” Type B, and Hepatitis B Field Guide. Washington, DC: Author, 2005.

Pascual, F. B., et al. “Tetanus Surveillance: United States, 1998–2000.” Morbidity and Mortality Weekly Report: Surveillance Summaries 52, no. 3 (June 20, 2003): 1–8.

"Tetanus." Mayo Clinic, April 24, 2013.

"Tetanus." MedlinePlus, November 22, 2011.

Traverso, H. P., et al. “A Reassessment of Risk Factors for Neonatal Tetanus.” Bulletin of the World Health Organization 69, no. 5 (1991): 573–79.

Worf, Neil. “Tetanus—Still a Problem.” RN 63, no. 6 (June, 2000): 44–49. N

What is stuttering? |

Causes and Symptoms

Stuttering is usually recognized as a child develops enough language skill to speak in complete sentences, beginning around three years of age. Typically, the child repeats the beginning sounds of a word, or whole words, before continuing with the sentence, as in, “I l-l-l-like to p-p-p-pet my ca-ca-cat.” True stuttering must be differentiated from developmental dysfluency and dysfluency caused by unusually severe environmental or social pressures. Developmental dysfluency is normal, occurring in the three- or four-year-old child whose brain works faster than his or her mouth. This child may repeat parts of words, words, or parts of phrases, especially when excited. When a child feels significantly anxious, language may become dysfluent, or broken up and difficult to understand. This is not true stuttering, and treatment should be aimed at alleviating the anxiety or stress.

True stuttering is less common than the two dysfluencies just described, and it occurs more often in boys. Frequently, the true stutterer is consistently dysfluent on the same sounds or words. There is consistency in repetitions, prolongations, pauses, grammatical forms, and rate of emission of dysfluency. Often, the child will overcome a verbal hurdle by using certain actions such as eye blinking, finger snapping, or foot tapping.

Treatment and Therapy

Treatment of true stuttering by a competent speech pathologist is imperative, and the prognosis, although variable, can be good. Parents and teachers should be alerted to alleviate any emotional stress that is unusual or severe. Absolutely essential is the ability of all adults to deal with the stuttering child without calling attention to the speech patterns or mannerisms. Practicing reading aloud, especially poetry, and singing—all in the privacy of the company of a caring adult—may help.

Perspective and Prospects

The great ancient Greek orator Demosthenes was dysfluent and allegedly practiced talking with pebbles in his mouth until he could speak clearly. Stuttering does not preclude a person becoming successful in any endeavor. Modern speech therapy and understanding adults can be of great benefit to a child who stutters. The 2010 film The King's Speech, which focused on King George VI of England's work with a speech therapist, stimulated public discussion of stuttering and its treatment. Colin Firth received an Academy Award for Best Actor for his portrayal of King George in the film.

Bibliography

Cole, Patricia R. Language Disorders in Preschool Children. Englewood Cliffs, N.J.: Prentice Hall, 1982.

Hamaguchi, Patricia McAleer. Childhood Speech, Language, and Listening Problems: What Every Parent Should Know. 2d ed. New York: Wiley, 2001.

Martin, Katherine L. Does My Child Have a Speech Problem? Chicago: Chicago Review Press, 1997.

Pinker, Steven. The Language Instinct: How the Mind Creates Language. New York: HarperCollins, 2007.

Plante, Elena, and Pelagie M. Beeson. Communication and Communication Disorders: A Clinical Introduction. 3d ed. Boston: Pearson/Allyn & Bacon, 2008.

Stuttering Foundation. http://www.stuttersfa.org.

What are the important things Martin Luther King wants his audience to know in his "I Have a Dream" speech?

In his "I Have a Dream" speech, Martin Luther King bases his thesis on two main ideas: (1) African Americans still are not free; and (2) now is the time for African Americans to fight for freedom. These are two critical points King wants his audience to know.Within the opening paragraphs of his speech, King references the Emancipation Proclamation, ratified by Abraham Lincoln during the Civil War to set slaves free. King...

In his "I Have a Dream" speech, Martin Luther King bases his thesis on two main ideas: (1) African Americans still are not free; and (2) now is the time for African Americans to fight for freedom. These are two critical points King wants his audience to know.

Within the opening paragraphs of his speech, King references the Emancipation Proclamation, ratified by Abraham Lincoln during the Civil War to set slaves free. King further points out that, "one hundred years" after the signing of the Emancipation Proclamation, the "Negro still is not free." The African American still was not free because he still suffered from racial discrimination, segregation, and poverty, preventing the African American from benefiting from the "Life, Liberty, and the pursuit of Happiness" promised by the Declaration of Independence.

King further warns his audience, especially his white audience members, against being foolish enough to believe that, now African Americans have had their day of protest, they "will now be content" to go back to their places of subordination. Instead, he argues that "[n]ow is the time" for African Americans to rise up against injustice. However, he also warns his people against using violence to achieve their goals and continues to promote peaceful protest.

What is neonatal jaundice? |

Causes and Symptoms

Most jaundice found in children is neonatal nonhemolytic
jaundice, a yellowish pigmentation of the skin of some infants. The term
“nonhemolytic” is used to differentiate this condition from jaundice caused by
blood group incompatibilities (such as Rh or ABO groups) or other enzyme
abnormalities of the red blood cells.

Neonatal nonhemolytic jaundice is the result of an excess of serum
bilirubin called hyperbilirubinemia. The pigment bilirubin
is derived from two major sources. One source is the normal destruction of
circulating red blood cells (erythrocytes). The normal life span of the
erythrocytes varies from 80 to 120 days. Old erythrocytes are removed and
destroyed in specific tissues in the spleen and liver, where the hemoglobin of the
red blood cells is broken down and converted to bilirubin. This accounts for about
75 percent of the daily production of bilirubin. The remaining 25 percent of
bilirubin is derived from ineffective erythropoiesis (red blood cell formation) in
the bone marrow and other tissue heme or heme proteins from the liver.

The bilirubin formed is transported in the plasma of the blood and bound
reversibly to albumin, a protein in the blood and tissues. This bilirubin-albumin
complex is then transported to the liver, where it is converted into a
water-soluble compound (or conjugated) by the enzyme glucuronyl transferase in the
interior of the liver cells. The conjugated bilirubin is excreted into the bile
capillaries and then into the intestine. Once in the small intestine, the
conjugated bilirubin is converted by bacteria in the colon into a colorless
compound known as urobilinogen. In the newborn infant, because of the lack of
bacteria in the colon and the presence of the enzyme
B-glucuronidase in the gut wall, a significant amount of the conjugated bilirubin
is deconjugated and reabsorbed back into the plasma pool, a process known as the
enterohepatic shunt.

Chemical hyperbilirubinemia can be defined as a serum concentration of bilirubin
that exceeds 1.5 milligrams per 100 milliliters. Visible yellowing (icterus) of
the skin is caused by the combination of normal skin color, bilirubin-albumin
complexes located outside the blood vessels, and precipitated bilirubin acid in
the membranes of the cell walls. It first becomes visible when serum bilirubin
reaches from 3 to 6 milligrams per deciliter, depending on the infant’s skin
texture and pigmentation and on the observer. Jaundice is first seen in the face
and eyes and then progresses toward the trunk and extremities.

In general, infants whose jaundice is restricted to the face and trunk and does
not extend below the umbilicus have serum bilirubin levels of about 12 milligrams
per deciliter or less, while those whose hands and feet are jaundiced have serum
bilirubin levels in excess of 15 milligrams per deciliter. A more objective way to
estimate the depth of jaundice in neonates is with the use of an icterometer, a
strip of transparent plastic with five transverse yellow strips in different
shades. The baby’s skin is blanched using pressure, and the resulting shade of
yellow is matched against a color scale. In recent years, a transcutaneous
bilirubinometer has been developed, which provides an electronic readout of an
index that corresponds with a serum bilirubin concentration. A more precise way to
judge jaundice is to draw a small amount of blood from the baby and to measure its
serum concentration in a laboratory.

A transient rise in serum bilirubin concentration is almost universally seen in
healthy newborns between one to seven days old. This type of jaundice, called
physiologic jaundice, may be attributable to several factors. First, this
condition may result from increased bilirubin load on liver cells caused by
increased red
blood cell volume, decreased red blood cell survival time,
increased heme from muscles, or increased enterohepatic circulation of bilirubin.
Second, the condition may result from decreased liver uptake of bilirubin from
plasma caused by a decrease in specific proteins in liver cells (termed Y and Z
proteins) for the transport of bilirubin. Third, it may result from defective
bilirubin conjugation caused by decreased enzyme activity. Fourth, physiologic
jaundice can result from defective bilirubin excretion.

The serum bilirubin level in newborns reaches its peak between three and five days
after birth and then decreases, so that the yellowish pigmentation may not be
visible by the fifth to seventh day. The peak level of serum bilirubin in
physiologic jaundice varies from a mean of 5 to 15 milligrams per 100 milliliters.
A number of factors will confound the level of serum bilirubin present with this
condition. They include maternal pregnancy history, complications, drugs,
gestational age, early initiation of feeding, type of feeding (breast milk or
formula), and ethnicity. The heterogeneity of the human population makes it
difficult to apply a particular serum bilirubin level to the definition of
physiologic jaundice. No jaundice should be dismissed as physiologic, however,
without at least a review of maternal and neonatal history, an examination of the
infant for signs of illness, and further laboratory investigation when
indicated.

In some cases, excess bilirubin can cause neurotoxicity leading to brain damage
known as bilirubin encephalopathy or kernicterus. This damage can result in either
neonatal death or the development of long-term abnormal neurologic findings, such
as cerebral
palsy, a low intelligence quotient (IQ), lower
school achievement, hyperactivity, and deafness. The identification of jaundiced
newborn infants at risk for kernicterus is difficult. The data suggest that
healthy infants with serum bilirubin levels as high as 25 to 30 milligrams per 100
milliliters may not have adverse neurologic effects, since the bilirubin is bound
to adequate albumin and the blood-brain barrier formed by cerebral blood vessels
is intact in these infants. Early hospital discharge policies practiced in many
maternity centers, however, make it difficult to assess the evolution of
physiologic as well as pathologic jaundice, or confounding factors such as
infection. Clinicians, practitioners, and home health visitors need to pay special
attention to the degree of jaundice and when it is associated with danger signs
such as sleepiness, lethargy, irritability, poor feeding, vomiting, fever,
high-pitched or shrill cry, hypertonia or hypotonia (depending on whether the
infant is asleep or awake), neck and trunk arching, dark urine, or light
stools.

Treatment and Therapy

The treatment of jaundice depends on the underlying pathology. For clinical
purposes, the two major types need to be separated: jaundice resulting from
hemolytic disease (Rh, ABO, and other blood group incompatibilities) and
nonhemolytic jaundice. Nonhemolytic jaundice may be physiologic or an accentuation
of physiologic jaundice, such as jaundice caused by polycythemia (an increased
number of red blood cells), cephalhematoma (the collection of blood in the scalp
between the bone and bone lining), bruising, cerebral or other hemorrhages,
swallowed blood, increased enterohepatic shunting (because of breastfeeding,
delayed passage of stools, or gastrointestinal tract obstruction), and infection
or sepsis.

Although no general consensus exists concerning the management of nonhemolytic
jaundice, infants with this condition are generally treated with phototherapy.
Phototherapy consists of exposure of the baby’s skin to light energy from a bank
of fluorescent, other special lamps, or sunlight. The light converts the
fat-soluble bilirubin, which cannot be excreted, into a water-soluble bilirubin,
which can be easily excreted in the bile, thus lowering the serum concentration of
bilirubin.

When the serum bilirubin level reaches between 20 and 25 milligrams per 100
milliliter—some clinicians advocate between 25 and 30 milligrams per 100
milliliters—exchange transfusion is generally recommended. In this method, all of
the baby’s bilirubin-containing blood is removed and exchanged with compatible
blood, without bilirubin, from a donor. Both forms of treatment, phototherapy and
exchange transfusion, aim to reduce or remove bilirubin from the baby’s system,
thereby preventing brain injury.

Perspective and Prospects

Jaundice was identified as a major problem in newborn infants in the nineteenth
century. Its association with brain injury was first described by German
pathologist Johannes J. Orth in 1875. Fifty years later, brain damage was further
identified with increased destruction of red blood cells because of
hemolysis caused by Rh and ABO blood group
incompatibilities.

It was also realized, however, that jaundice is encountered in healthy newborn
infants. The major problem has been to identify which infants are at risk for
brain damage when bilirubin is at a particular level. Since there are multiple
confounding factors, better means are being developed for identifying risks, such
as laboratory methods to identify free (unbound) bilirubin and noninvasive
clinical methods such as auditory evoked potential to measure brain waves in
response to sound and nuclear magnetic resonance to measure the energy metabolism
of brain cells. In addition, methods to prevent the formation of bilirubin or to
reduce its levels by decreasing the activity of the enzyme heme oxygenase are
being studied.

Bibliography

Behrman, Richard E.,
Robert M. Kliegman, and Hal B. Jenson, eds. Nelson Textbook of
Pediatrics. 19th ed. Philadelphia: Saunders/Elsevier, 2011.
Print.

Kirchner, Jeffrey T.
“Clinical Assessment of Neonatal Jaundice.” American Family
Physician 62.8 (2000): 1880. Print.

MacDonald, Mhairi G.,
Mary M. K. Seshia, and Martha D. Mullett, eds. Avery’s Neonatology:
Pathophysiology and Management of the Newborn. 6th ed.
Philadelphia: Lippincott, 2005. Print.

Martin, Richard J.,
Avroy A. Fanaroff, and Michele C. Walsh, eds. Fanaroff and Martin’s
Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. 2
vols. 9th ed. Philadelphia: Mosby/Elsevier, 2011. Print.

In what ways has the house infantilized the Hadleys in "The Veldt"? How does Bradbury depict this as dangerous?

George and Lydia's Happylife Home plays a number of roles in the story -- not least, it can be understood as the true antagonist, the force that undermines their parental authority and drives a wedge between them and their children. It has "infantalized" the parents, no doubt -- but if the parents have been turned into children, then it makes sense to ask what sort of "parent" the house can be. If you think about it that way, you can begin to see the shape of the satire at work in Bradbury's story. 

First, the basic thing about the house is that it does everything for you. The Happylife home is the ultimate expression of the labor-saving device: the home that "clothed and fed and rocked them to sleep and played and sang and was good to them." Lydia feels unnecessary, as you say: "That's just it. I feel like I don't belong here. The house is wife and mother now, and nursemaid." She wants to take a "vacation," which, oddly, means a return to domestic drudgery: she wants to be the one frying eggs, darning socks, sweeping the floor. 

Lydia's desire to do these things comes from her sense that the house has replaced her as mother; her assumption that "darning socks" is what makes a mother is of course another expression of her infantilization. Lydia longs to "go back" to being a mother, but it is clear that, in real terms, she doesn't know what that means -- cooking breakfast is not the same as having a emotional bond with your children, and, of course, that bond is exactly what is missing.

Second, the house satirizes the "leisure first" lifestyle Americans value to this day. The fact that the house will make dinner and tie your shoes is, on the face of it, a ridiculous exaggeration. But Bradbury is also indicting a society that confuses freedom from chores with freedom from responsibility. Perhaps the real reason George and Lydia are unhappy in the house is because of what it doesn't do -- absolve them of guilt for not connecting with their children. 

Third, the house infantalizes the parents in that it becomes the means for their children to assume the role of "head of household." That is, the suggestion is that the kids have hacked the house somehow (Peter may have "got into the machinery and fixed something"). George, who admires the technical acheivement of the house, really has no idea how it works. Lydia is childishly afraid of the nursery ("Those lions can't get out of there, can they?" she asks at one point). The parents fear the children, and fear that they have become more powerful than they are. 

Of course, the children become more powerful than the parents. That's what kids do: they grow up. I think, in the end, the house infantilizes the parents because it shows that the parents don't know, really, what being a parent is: someone that helps their children grow up. In the end, the house provides on last labor saving service: it gets rid of the parents altogether.

How did Thomas Dixon's book The Clansman and D.W. Griffith's film The Birth of a Nation change the story of African-Americans? This question is...

On page 216 of David S. Reynold's Mightier Than the Sword, the author writes that Dixon, the author of The Clansman (1903), was "disgusted by Stowe." Dixon blamed Stowe for starting the Civil War. In reaction to Stowe's abolitionist novel Uncle Tom's Cabin, Dixon set out to write the story of the Civl War and Reconstruction from the southern perspective. His view was that Reconstruction was a failure. 

Similar to other pseudoscientific thinkers...

On page 216 of David S. Reynold's Mightier Than the Sword, the author writes that Dixon, the author of The Clansman (1903), was "disgusted by Stowe." Dixon blamed Stowe for starting the Civil War. In reaction to Stowe's abolitionist novel Uncle Tom's Cabin, Dixon set out to write the story of the Civl War and Reconstruction from the southern perspective. His view was that Reconstruction was a failure. 

Similar to other pseudoscientific thinkers of the day, such as John Carroll, who wrote The Negro a Beast in 1900, Dixon saw African-Americans as no better than animals, driven by animal-like instincts and possessing little intellectual power. He thought African-American men posed a threat to white women, and Dixon reinforced these ideas in his trilogy about the Klan. The Clansman was one of the novels in this trilogy. In his novel, a white girl is raped by a black man in the presence of her mother, and the girl and her mother kill themselves in humiliation. His novel inspired the D.W. Griffith silent film Birth of A Nation of 1915, for which Dixon was an advisor. This film portrayed the Civil War and Reconstruction as failures and reinforced the Dunning school of historiography, which also publicized the idea that Reconstruction was a failed effort. The film portrayed African-Americans as incapable of leading the south after the Civil War. The film also portrayed the Klan as heroes who restored the south to glory.