What is human growth hormone?

Growth Hormones and Disease Symptoms

The pituitary (hypophysis) is an acorn-sized gland located at the base of the brain that makes important hormones and disseminates stored hypothalamic hormones. The hypothalamus controls the activity of the pituitary gland by sending signals along a network of blood vessels and nerves that connects them. The main portion of the pituitary gland, the adenohypophysis, makes six trophic hormones that control many body processes by causing other endocrine glands to produce hormones. The neurohypophysis, the remainder of the pituitary, stores two hypothalamic hormones for dissemination.

Dwarfism
is caused by the inability to produce growth hormone. When humans lack only human growth hormone (HGH), resultant dwarfs have normal to superior intelligence. However, if the pituitary gland is surgically removed (hypophysectomy), the absence of other pituitary hormones causes additional mental and gender problems. The symptoms of dwarfism are inability to grow at a normal rate or attain adult size. Many dwarfs are two to three feet tall. In contrast, some giants have reached heights of more than eight feet. The advent of gigantism
often begins with babies born with pituitary tumors that cause the production of too much HGH, resulting in continued excess growth. People who begin oversecreting HGH as adults (also caused by tumors) do not grow taller. However, the bones in their feet, hands, skull, and brow ridges overgrow, causing disfigurement and pain, a condition known as acromegaly.

Dwarfism that is uncomplicated by the absence of other pituitary hormones is treated with growth hormone injections. Humans undergoing such therapy can be treated with growth hormones from humans or primates. Growth hormone from all species is a protein made of approximately two hundred amino acids strung into a chain of complex shape. However, differences in amino acids and chain arrangement in different species cause shape differences; therefore, growth hormone used for treatment must be extracted from a related species. Treatment for acromegaly and gigantism involves the removal of the tumor. In cases where it is necessary to remove the entire pituitary gland, other hormones must be given in addition to HGH. Their replacement is relatively simple. Such hormones usually come from animals. For many years, the sole source of HGH was pituitaries donated to science. This provided the ability to treat fewer than one thousand individuals per year. Molecular genetics has solved that problem by devising the means to manufacture large amounts of transgenic HGH.

Growth Hormone Operation and Genetics

In the mid-1940s, growth hormone was isolated and used to explain why pituitary extracts increase growth. One process associated with HGH action involves cartilage cells at the ends of long bones (such as those in arms and legs). HGH injection causes these epiphysial plate cells (EPCs) to rapidly reproduce and stack up. The EPCs then die and leave a layer of protein, which becomes bone. From this it has been concluded that growth hormone acts to cause all body bones to grow until adult size is reached. It is unclear why animals and humans from one family exhibit adult size variation. The differences are thought to be genetic and related to production and cooperation of HGH, other hormones, and growth factors.

Genetic research has produced transgenic HGH in bacteria through the use of genetic engineering technology. The gene that codes for HGH is spliced into a special circular piece of DNA called a plasmid expression vector, thus producing a recombinant expression vector. This recombinant vector is then put into bacterial cells, where the bacteria express the HGH gene. These transgenic bacteria can then be grown on an industrial scale. After bacterial growth ends, a huge number of cells are harvested and HGH is isolated. This method enables isolation of enough HGH to treat anyone who needs it.

Impact and Applications

One use of transgenic HGH is the treatment of acromegaly, dwarfism, and gigantism. The availability of large quantities of HGH has also led to other biomedical advances in growth and endocrinology. For example, growth hormone does not affect EPCs in tissue culture. Ensuing research, first with animal growth hormone and later with HGH, uncovered the EPC stimulant somatomedin. Somatomedin stimulates growth in other tissues as well and belongs to a protein group called insulin-like growth factors. Many researchers have concluded that the small size of women compared to men is caused by estrogen-diminished somatomedin action on EPCs. Estrogen, however, stimulates female reproductive system growth by interacting with other insulin-like growth factors.

Another interesting experiment involving HGH and genetic engineering is the production of rat-sized mice. This venture, accomplished by putting the HGH gene into a mouse chromosome, has important implications for understanding such mysteries as the basis for species specificity of growth hormones and maximum size control for all organisms. Hence, experiments with HGH and advancements in genetic engineering technology have led to, and should continue to lead to, valuable insights into the study of growth and other aspects of life science.

Key terms




endocrine gland


:

a gland that secretes hormones into the circulatory system




hypophysectomy

:

surgical removal of the pituitary gland





pituitary gland


:

an endocrine gland located at the base of the brain; also called the hypophysis




transgenic protein

:

a protein produced by an organism using a gene that was derived from another organism





Bibliography

“Can We Prevent Aging? Tips from the National Institute on Aging.” National Institute on Aging. US Department of Health and Human Services, June 2010. Web. 4 Aug. 2014.

Cohen, Susan, and Christine Cosgrove. Normal at Any Cost: Tall Girls, Short Boys, and the Medical Industry’s Quest to Manipulate Height. New York: Tarcher, 2009. Print.

Eiholzer, Urs. Prader-Willi Syndrome: Effects of Human Growth Hormone Treatment. New York: Karger, 2001. Print.

Flyvbjerg, Allan, Hans Orskov, and George Alberti, eds. Growth Hormone and Insulin-Like Growth Factor I in Human and Experimental Diabetes. New York: Wiley, 1993. Print.

Ho, Ken. Growth Hormone Related Diseases and Therapy: A Molecular and Physiological Perspective for the Clinician. New York: Humana, 2011. Print.

Jorgensen, Jens Otto Lunde, and Jens Sandahl Christiansen, eds. Growth Hormone Deficiency in Adults. New York: Karger, 2005. Print.

Shiverick, Kathleen T., and Arlan L. Rosenbloom, eds. Human Growth Hormone Pharmacology: Basic and Clinical Aspects. Boca Raton: CRC, 1995. Print.

Smith, Roy G., and Michael O. Thorner, eds. Human Growth Hormone: Research and Clinical Practice. Totowa: Humana, 2000. Print.

Ulijaszek, J. S., M. Preece, and S. J. Ulijaszek. The Cambridge Encyclopedia of Human Growth and Development Growth Standards. New York: Cambridge UP, 1998. Print.

Williams, Mary E. Growth Disorders. Farmington Hills: Greenhaven, 2012. Print.

What are some quotes showing why Helen Robinson can't get a job?

Scout first learns about Helen Robinson not being able to find work in Maycomb County in chapter 12 when she goes with Jem to Calpurnia's church. At the end of Reverend Sykes' sermon, he asks the congregation to give money for Helen Robinson in the collection can. After the first go-around, there isn't as much money as Reverend Sykes wanted. He wants to collect ten dollars. In an effort to collect more money he says...

Scout first learns about Helen Robinson not being able to find work in Maycomb County in chapter 12 when she goes with Jem to Calpurnia's church. At the end of Reverend Sykes' sermon, he asks the congregation to give money for Helen Robinson in the collection can. After the first go-around, there isn't as much money as Reverend Sykes wanted. He wants to collect ten dollars. In an effort to collect more money he says the following:

"You all know what it's for—Helen can't leave those children to work while Tom's in jail. If everybody gives one more dime, we'll have it" (122).

Scout wonders why this is the case for Helen because many African American mothers take their children along with them to the fields when they work. Scout asks the Reverend about it. He responds with the following:

"To tell you the truth, Miss Jean Louise, Helen's finding it hard to get work these days. . . when it's picking time, I think Mr. Link Deas'll take her" (123).

This still makes Scout wonder, so she turns to Calpurnia for another answer to why Helen can't get work. Calpurnia says this:

"It's because of what folks say Tom's done . . . Folks aren't anxious to—to have anything to do with any of his family" (123).

Then Scout gets a watered-down version of how Tom got put in jail, but Cal won't give her the definition of rape. The point is that Scout discovers that Helen isn't finding work because people are shunning her for what her husband allegedly did.

What is bubonic plague? |

Definition

Bubonic plague is a severe bacterial infection characterized by acute, local, necrotizing lymphadenitis (infection of the lymph glands). Bacteremia rapidly follows, then spreads to the spleen, liver, and other organs. Bubonic plague is the most common form of plague and has a mortality rate of 50 to 90 percent if not treated. If treated promptly and appropriately, the mortality rate is 5 to 15 percent.

Bubonic plague is one of the oldest diseases known and has been one of the most devastating in human history. It is widely regarded as a disease of mainly historical importance because it is now rare in developed countries and affects mainly poor and remote populations. However, reports of incidence have increased once again.

In Madagascar, Peru, and the Democratic Republic of the Congo, bubonic plague is a significant health concern. Adding to the new incidence rate is the discovery of antibiotic-resistant strains of the plague bacterium. The Centers for Disease Control and Prevention reports that as of 2015, an average of seven human cases develop each year in the United States, with the highest incidence occurring in the southwestern states of New Mexico, Arizona, and Colorado. According to the American Society of Tropical Medicine and Hygiene, between 2000 and 2009, more than 20,000 cases of humans infected with the plague were reported worldwide, with the following countries having the highest incidences (in order of most reported cases): DRC, Madagascar, Zambia, Uganda, Mozambique, Tanzania, China, Peru, Malawi, Indonesia, the United States, and Vietnam. The World Health Organization WHO) concedes that official data on the plague do not truly reflect incidence of plague, mainly because of a reluctance to report plague cases but also because of inadequate surveillance capabilities.

Causes

Bubonic plague is caused by the bacterium Yersinia pestis (formerly called Pasteurella pestis). Alexandre Yersin isolated the bacterium (germ) that causes plague. (The bacterium was named Y. pestis for Yersin.) He developed a treatment (an antiserum) to combat the disease and was the first to suggest that fleas and rats may have spread plague in the epidemic of 1894. Y. pestis is a nonmotile, non-acid-fast, non-spore-forming, gram-negative coccobacillus (bacterium) measuring 1.5 by 0.75 microns. The bacterium can be killed in less than ten minutes with sunlight, high temperatures, desiccation, ordinary disinfectants, and preparations containing chlorine.

Y. pestis is primarily an internal parasite of wild rodents. It is transmitted by rat fleas from wild rodents to domestic rats (Rattus norvegicus and especially R. rattus)
and then to humans (or directly from wild rodent to human). Y.
pestis reproduces rapidly in the wild rodent, which may then be
overcome with sepsis. A vector transmits it to a human from the wild
rodent. The vector is usually a rat flea of the species Xenopsylla cheopis, X. ramesis, or X.
nubica, although thirty different flea species have been identified as
carriers of plague; other vectors include ticks and
human
lice.

The vector takes a blood meal from the rodent, sucking up large amounts of Y. pestis bacteria, which then establish a colony in the stomachs and esophagi of some of these fleas. As a result, the flea cannot fit blood into its stomach and thus becomes extremely hungry. This extreme hunger drives the flea into intense blood-sucking (hematophagia). To avoid starvation, it will seek a blood meal from any nearby host, such as a human, rather than seek out a preferred rodent. This “blocked” flea will suck voraciously until it involuntarily regurgitates some of the blood it is sucking and some of the bacilli. As the flea feeds, it also defecates and thus excretes bacilli onto the human skin. The person scratches at the flea bite and thus deposits Y. pestis into his or her bloodstream.

As soon as a rodent that is infected with plague dies, its fleas leave for living hosts, humans often being the only nearby alternative. Under optimal conditions, vector fleas can live for six weeks, but they probably can transmit plague for about two weeks only. X. cheopis, the flea species most likely to transmit plague, flourishes in a dry, warm environment of about 60° to 77° Fahrenheit (20° to 25° Celsius). Bubonic plague can persist in relatively small rodent populations from which occasional human epidemics then arise.

Y. pestis probably evolved from the Central Asiatic plateau, the swathe of desert that reaches across Central Asia, the Middle East, and North Africa. It is rich with rodents and fleas that harbor and transmit plague. It is possible that these animals transferred Y. pestis from Central Asia to North Africa and subsequently to Central Africa.

The human flea (Pulex irritans) may be a transmitter of plague in some areas of Africa. However, human-to-human transmission of bubonic plague is uncommon because Y. pestis rarely produces in humans the level of sepsis needed for a flea to become blocked and thereby become a vector for bubonic plague.

Transmission can also occur when a person inhales plague-infected organisms
that have been released into the air. The inhalation form of the plague can be
aerosolized and used in acts of bioterrorism.

Risk Factors

The main risk factor for bubonic plague is contact with rodents carrying infected fleas. This may occur through occupational or environmental exposure to rats, ferrets, rabbits, squirrels, marmots, gerbils, birds, prairie dogs, bobcats, and coyotes. More than two hundred different rodents and other species can serve as hosts. Recent flea bites and scratches or bites from infected domestic cats are also risk factors.

Risk factors may be heightened by environmental and cultural conditions. For example, the Alur ethnic group in the West Nile region store grain and livestock in the same structure where people sleep because of the possibility of theft. This, coupled with the cultural practice of gathering and sleeping in the home of a deceased for three or four days (as dictated by the belief that the deceased spirit lingers and should be recognized by surviving relatives and friends), may increase the risk of contracting plague. An unusually prolonged drought is another risk factor because it may force field rodents to seek food in buildings. Poverty, poor sanitation, and poor food-storage practices are also risk factors. Late diagnosis is a risk factor for the spread of bubonic plague because it limits the effectiveness of control measures.

Symptoms

The classic symptom of bubonic plague appears usually one to six days after exposure as a smooth and painful lymph gland swelling known as a bubo. A bubo is most commonly found in the groin but is also found in the armpits and neck. A bubo usually occurs at the site of the initial flea bite or scratch. Pain may occur at the site before the bubo appears. If the infected person survives, the bubo usually suppurates in one to two weeks because of secondary infection with pyogenic bacteria. It may then burst and leave a deep ulcer. Other symptoms of bubonic plague are malaise (a general ill feeling), myalgia (muscle aches and pain), high fever, chills, severe headache, nausea, vomiting, seizures, and prostration. Petechiae (purplish spots caused by small hemorrhages); ecchymoses (purple discoloration from ruptured blood vessels); bleeding into the tissues, which turns the tissue black; and bleeding from the gastrointestinal tract may also present. In its mild form, however, bubonic plague may not even confine a person to bed.

If left untreated, bubonic plague can became septicemic or pneumonic plague, which affect the blood stream and the lungs, respectively. In addition to the other symptoms of bubonic plague, shock may occur with septicemic plague or pneumonic plague. Pneumonic plague is characterized by respiratory symptoms such as cough, chest pain, thin or bloody mucus excretions, shortness of breath, and even respiratory failure. When someone has pneumonic plague, the disease can also transmit directly to another human through airborne droplets.

Screening and Diagnosis

A doctor will ask the patient about symptoms and medical history and will perform a physical examination. Diagnostic tests may include blood and urine samples, sputum samples, a chest X ray, a computed tomography (CT) scan, a magnetic resonance imaging (MRI) scan, and a bronchoscopy, in which a thin scope is used to look into the lungs. Laboratory confirmation includes cultures from samples of blood, sputum, and fluid from the bubo. Cultures require more than forty-eight hours to produce definitive results. If plague infection is discovered, an infectious disease specialist should be contacted for assistance.

Treatment and Therapy

One should immediately treat suspected bubonic plague with antibiotics and then initiate confirmatory laboratory work. Without prompt treatment, Y. pestis can multiply in the bloodstream or spread to the lungs so rapidly that it may lead to the more serious pneumonic plague. Persons with bubonic plague are often hospitalized and placed in isolation, however.

The standard treatment for bubonic plague is intramuscular streptomycin (1 gram twice daily for ten days). Less severe cases can be treated with 500 milligrams (mg) of oral tetracycline, four times daily. Chloramphenicol is a suitable alternative and is administered in divided doses of 50 mg per kilogram per day, either parenterally or, if tolerated, orally for ten days. Gentamycin is the preferred antibiotic for treatment during pregnancy because it is safe, because it can be administered either intravenously or intramuscularly, and because its concentrations in the blood can be monitored.

The three most effective drugs have potentially serious adverse events associated with use during pregnancy: streptomycin may be ototoxic and nephrotoxic to the fetus, tetracycline has an adverse effect on the developing teeth and bones of the fetus, and chloramphenicol carries a risk, albeit low, of gray baby syndrome or bone-marrow suppression. Sulfonamides have been used extensively in plague treatment; however, some studies have shown higher mortality, increased complications, and longer duration of fever with its use compared with treatment with streptomycin, tetracycline, or chloramphenicol.

Prevention and Outcomes

Killed bacteria began to be used in plague vaccines in 1896. However, the vaccine licensed for use in the United States was a whole-cell bacterial vaccine, inactivated with formaldehyde and preserved in phenol. The primary series consisted of three doses: the first dose at the initial visit, the second dose one to three months later, and the third dose five or six months later. Booster doses could be given at six-month intervals if exposure continued. Common side effects included mild pain, erythema (redness), and induration (hardening) at the injection site. Fever, headache, and malaise were more common and more severe following repeated doses. Rare side effects included difficulty in breathing or swallowing; hives; itching, especially of soles or palms; reddening of skin, especially around ears; swelling of eyes, face, or inside of nose; and unusual, sudden, and severe tiredness or weakness. The plague vaccine was not very effective, however.

In 2000, the United States began working with Great Britain and Canada in sharing information about plague vaccine. In 2005, the three countries agreed to pool their resources to create a vaccine that combines the existing vaccine for the bubonic plague with a new kind of protection from the pneumonic plague. As of 2015, no plague vaccine was available to the public. In 2008, researchers from the Institut Pasteur in Paris used the less virulent ancestor to Y. pestis, Y. pseudotuberculosis, to try to develop a potentially safer, more efficient, and less expensive live oral vaccine. As of 2015, their efforts to create a stable, safe live vaccine remained ongoing.

Because human plague is rare in most parts of the world, there is no need to vaccinate anyone other than those at particularly high risk of exposure—namely, laboratory and field personnel working with or in proximity to Y. pestis. This intramuscular vaccine is not indicated for most travelers to countries reporting cases, particularly those traveling only to urban areas with modern hotel accommodations.

If a person is diagnosed with plague, most countries require that a governmental health agency be notified. Particularly if pneumonic plague is suspected, the person is kept in strict isolation until the disease is controlled with antibiotics. It is imperative that those who have been in close contact with an infected person be traced, identified, and evaluated. Infected persons might also be put under observation or given preventive antibiotic therapy (with a tetracycline, chloramphenicol, or one of the effective sulfonamides), depending on the degree and timing of contact. Antibiotics can also be given for a brief period to people who have been exposed to the bites of potentially infected rodent fleas or who have handled an animal known to be infected. People who must be present in an area where a plague outbreak is occurring can protect themselves for two to three weeks by taking antibiotics.

Many cities, especially in the United States, have instituted rodent-control programs because rodents also carry rabies and other deadly diseases. In rural areas, eliminating wild-rodent harborage and food sources and clearing brush, rock piles, and junk puts distance between rodents and the home. Ridding pet dogs and cats of fleas regularly prevents the fleas from jumping to other pets. Applying insect repellents, if available, to clothing and skin to prevent flea bites is advisable, as is wearing gloves when handling potentially infected animals. Keeping floors clean and occasionally pouring boiling water on a dirt floor and not sleeping on it is helpful.

In Africa, plague control is often reactive, not proactive, because of a lack of resources for surveillance. Plague control that targets rodents in Africa has focused on trapping, burning homes, and dusting homes and rodent burrows with powdered insecticide or other poisons such as dichloro-diphenyl-trichloroethane (DDT) powder followed by anticoagulant bait. Many countries employ rigorous disinfection routines for ships, docks, and aircraft because transportation of infected rodents aboard transcontinental vehicles has led to earlier pandemics.

Bibliography

Bahmanyar, M., and D. C. Cavanaugh. Plague Manual. Geneva: World Health Organization, 1999.

Borchert, Jeff N., Jeff J. Mach, and Timothy J. Linder. “Invasive Rats and Bubonic Plague in Northwest Uganda.” In Managing Vertebrate Invasive Species, edited by G. W. Witmer, W. C. Pitt, and K. A. Fagerstone. Fort Collins, Colo.: National Wildlife Research Center, 2007.

Cook, Gordon C., and Alimuddin I. Zumla, eds. Manson’s Tropical Diseases. 22d ed. Philadelphia: Saunders/Elsevier, 2009.

"Fast Facts on Plague in the 21st Century." ASTMH. Amer. Soc. of Tropical Medicine & Hygiene, n.d. Web. 29 Dec. 2015.

Findlay, John, and Drew Shrewsbury. A History of Bubonic Plague in the British Isles. New York: Cambridge University Press, 2005.

Jong, Elaine C., and Russell McMullen, eds. Travel and Tropical Medicine Manual. 4th ed. Philadelphia: Saunders/Elsevier, 2008.

Mandell, Gerald L., John E. Bennett, and Raphael Dolin, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. New York: Churchill Livingstone/Elsevier, 2010.

Marquardt, William C., ed. Biology of Disease Vectors. 2d ed. New York: Academic Press/Elsevier, 2005.

National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD). "Plague: Frequently Asked Questions." CDC. Centers for Disease Control and Prevention, 14 Sept. 2015. Web. 29 Dec. 2015.

What is laryngitis? |

Causes and Symptoms

The larynx, located directly above the windpipe (trachea), is the short, hollow tube containing the vocal cords,
two heavily lined slits in a mucous membrane. Voiced sounds, such as vowels, result when air from the lungs induces vocal fold vibration. Laryngitis occurs when the folds are obstructed or do not vibrate properly; depending on the cause, laryngitis is classified as simple, chronic, diphtheritic, tuberculous, or syphilitic.

Simple laryngitis may be caused by bacterial infection (common cold, typhoid fever), a virus (influenza), or nonbacterial irritants (chemical fumes, dust, or tobacco smoke). The primary infection site is the mucous membrane lining the larynx. It becomes red and swollen, secreting a viscous discharge that impedes vocal fold vibration. In severe cases of viral infection, the larynx may become completely obstructed, causing suffocation.

Chronic laryngitis often results from excessive smoking, alcoholism, or consistent strain or abuse of the voice. It is an occupational hazard of auctioneers, orators, singers, and those who frequently shout for long periods, such as cheerleaders. Nondisease-induced chronic laryngitis may also be instigated by hysteria, allergic reaction, remote disease of the nerves serving the voice, strong external pressure against the larynx, or irritation caused by tubes inserted down the throat to sustain breathing.

Diphtheritic laryngitis occurs when diphtheria
afflicting the upper throat spreads to the larynx. The result may be a membrane of diseased cells infiltrating the mucous membrane and obstructing the vocal cords.

Tuberculous laryngitis is a secondary infection spread from the lungs. Tubular nodulelike growths are formed in larynx tissue, leaving ulcers on the surface. Starting at the vocal cords, this infection may spread over the entire larynx and eventually destroy the epiglottis and laryngeal cartilage.

Syphilitic laryngitis is one of the many complications of syphilis. Sores or mucous patches form in the larynx, eventually producing tissue destruction and scar formation. The mucous membrane becomes dry and covered with polyps (small bumps of tissue that project from the surface). These polyps distort the larynx, shorten the vocal cords, and produce persistent hoarseness.

Treatment and Therapy

Simple laryngitis is best treated by resting the voice. When it is absolutely necessary to speak, it should be with a soft, breathy voice, not a whisper. The throat should be kept well lubricated by frequent drinks of water and not cleared. Relative humidity in the recovery room should be maintained at 40 to 50 percent, and alcohol, tobacco, and decongestants should be avoided. Complete recovery usually occurs within several days.

A persistent hoarseness indicates a bacterial infection (usually curable by antibiotics) or polyps, cysts, or other fibrous growths on the vocal cords. These growths may become ulcerated and require surgical intervention. Although cancer of the larynx is not uncommon (2 percent of malignancies), it is usually completely curable if detected sufficiently early.

Systemic diseases not localized in the larynx, such as tuberculosis and syphilis, are best treated by antibiotics.

Bibliography:

Bellenir, Karen, and Peter D. Dresser, eds. Contagious and Noncontagious Infectious Diseases Sourcebook. Detroit, Mich.: Omnigraphics, 1996.

Colton, Raymond H., Janina K. Casper, and Rebecca Leonard. Understanding Voice Problems: A Physiological Perspective for Diagnosis and Treatment. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2006.

Icon Health. Laryngitis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, Calif.: Icon Health, 2004.

LaRusso, Laurie. "Laryngitis." Health Library, January 9, 2013.

Mayo Clinic. "Laryngitis." Mayo Clinic, June 28, 2012.

Ossoff, Robert H., et al., eds. The Larynx. Philadelphia: Lippincott Williams & Wilkins, 2003.

Sataloff, Robert T., ed. Reflux Laryngitis and Related Disorders. 4th ed. San Diego, Calif.: Plural, 2013.

Swartzberg, John Edward. Wellness Self-Care Handbook: The Everyday Guide to Prevention and Home Remedies to Over 150 Common Ailments. New York: Times Books, 1999.

What are smoking's effects on the body?

Short-term Effects

A major reason for the spread and popularity of tobacco since the sixteenth century is connected to one of its short-term effects on the human body. An important active ingredient in tobacco smoke is nicotine, which is rapidly delivered into the bloodstream through the lungs. Nicotine is then transported to receptors in the central nervous system, increasing heart rate and the release of dopamine, a pleasure-inducing chemical. Tobacco smoke also contains chemical substances that increase heart rate and elevate blood pressure, sometimes causing dizziness and tremors because of a reduced flow of oxygenated blood to the brain and extremities.

Smoking also has short-term effects on the respiratory and digestive systems. Research on animals and humans has demonstrated that inhaling smoke from cigarettes impairs pulmonary clearance, which can lead to coughing and increased susceptibility to colds and allergens. Smoking attenuates the functioning of the lung’s cilia and alveoli, reducing the lung’s ability to oxygenate blood.

With regard to the digestive system, studies indicate that components of cigarette smoke foster increased acidity in the stomach, while other studies show that smoking may exacerbate gastric and duodenal ulcers. Deceptive advertisers have at times created the impression that one of the beneficial aspects of smoking is appetite reduction, instilling the fear that cessation of smoking will lead to weight gain. Many researchers, however, insist this fear must be directly opposed because documented weight gain after cessation has complex causes.

The body’s nervous, muscular, and reproductive systems are quickly affected by certain components in tobacco smoke. Because nicotine readily passes through the blood-brain barrier, it stimulates certain receptors that in novice smokers may induce nausea. In experienced smokers, however, this fact may explain why, with various physiological changes, some of them pleasurable, smoking becomes a deeply entrenched habit. Much research indicates that nicotine plays a significant role in establishing the smoking habit, though some smokers become dependent on nicotine-free cigarettes.

Because of smoking’s negative effects on the muscular system, athletes have been perennially warned about smoking’s ability to impair performance. Also, extensive research has been done on the immediate effects of smoking during pregnancy and the multiple harmful chemicals in cigarette smoke on the fetuses of animals and humans. These chemicals cause such effects as changes in fetal heart rate and placental circulation and metabolism; a rise in carboxyhemoglobin concentrations; and a host of other problems, which have led to a series of warnings that pregnant women should not smoke.

Long-Term Effects

Scientific research has revealed that smokers are exchanging short-term pleasures for a devastating array of extremely negative long-term health consequences, including chronic problems for the circulatory, respiratory, and other bodily systems. Extensive research has shown habitual smoking dramatically increases the risk for arteriosclerosis and coronary heart disease. General agreement exists that acute and chronic cardiovascular effects of smoking can be largely attributed to nicotine. Smoking also has been associated with narrowing of the blood vessels in the heart, brain, and other organs, significantly increasing the chances of stroke.

According to some analysts, the body’s respiratory system experiences the most devastating damage from long-term smoking. Evidence shows a causal relationship between smoking and lung cancer, and that smokers are more than ten times as likely as nonsmokers to have lung cancer. These studies also indicate that more than 90 percent of all lung-cancer cases in men, and 80 percent in women, are caused by smoking. Furthermore, habitual smoking has been associated with increased susceptibility to such chronic obstructive pulmonary diseases as emphysema and bronchitis. According to the US Centers for Disease Control and Prevention, men who smoke increase their risk of dying from bronchitis and emphysema by seventeen times.

Because smoking reduces the effectiveness of the body’s immune system, habitual smokers readily have a variety of respiratory infections, including pneumonia. Other research has established a causal relationship between smoking and cancers of the digestive and urinary systems. For example, smokers are much more likely to develop and die from mouth and throat cancers, stomach cancers, colorectal cancer, pancreatic cancers, bladder cancer, and kidney cancer. Indeed, several analysts believe that 30 to 50 percent of all cancer deaths in the United States can be directly attributed to smoking. Worldwide, tobacco use causes nearly six million deaths each year. Smokers die an average of ten years earlier than nonsmokers.

Much research has been devoted to studying the long-term health effects of smoking on the reproductive system. These studies have revealed negative effects from fertilization to birth. Smoking causes lowered fertility; stunted fetal growth; increased likelihood of miscarriages, premature births, and stillbirths; and complications for normal-term births. Women who are habitual smokers also give birth to babies with low birth weights, and the harmful chemicals in the bodies of breastfeeding mothers who are smoking can be passed to their babies, causing immediate and long-term damage. The reproductive systems of men also are affected by smoking, with reduced sperm count and increased impotency the most commonly reported problems.

Although the negative cosmetic effects of smoking are not as serious as the effects on the major systems of the body, they have, nevertheless, been studied. For example, smoking leads to premature aging of the skin, chiefly by interfering with the collagen production involved in renewing skin. Habitual smoking often results in bad breath, stained teeth, discolored fingers, and an unhealthy complexion.

Because of all the short- and long-term effects of smoking on the body, various institutions, including the World Health Organization, the US Office of the Surgeon General, and the American Heart Association, have persistently urged smokers to quit so that they might enjoy longer, healthier lives.

Bibliography

Brandt, Allan M. The Cigarette Century: The Rise, Fall, and Deadly Persistence of the Product That Defined America. New York: Basic, 2007. Print.

Glantz, Stanton A., et al. The Cigarette Papers. Berkeley: U of California P, 1996. Print.

How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Rockville: DHHS, 2010. Print.

Lock, Stephen, Lois Reynolds, and E. M. Tansey. Ashes to Ashes: The History of Smoking and Health. Atlanta: Rodopi, 1998. Print.

Siegel, Rebecca L., et al. "Deaths Due to Cigarette Smoking for 12 Smoking-Related Cancers in the United States." JAMA Internal Medicine 175.9 (2015): 1574–76. Print.

"Smoking and Tobacco Use: Fast Facts." Centers for Disease Control and Prevention. US Dept. of Health and Human Services, 15 Apr. 2015. Web. 29 Oct. 2015.

"Smoking and Tobacco Use: Health Effects of Cigarette Smoking." Centers for Disease Control and Prevention. US Dept. of Health and Human Services, 1 Oct. 2015. Web. 29 Oct. 2015.

"Smoking and Tobacco Use: Smoking-Related Mortality." Centers for Disease Control and Prevention. US Dept. of Health and Human Services, 18 Apr. 2015. Web. 29 Oct. 2015.

How does screening for behavioral addiction work?

Introduction

Behavioral addictions are patterns of behavior that follow a cycle similar to that of chemical addiction. Persons addicted to certain behaviors, such as gambling, exercising, computer gaming, Internet use, shopping, eating, or sexual activity, crave the activity and engage in that activity at the risk of causing problems in important life areas.

Behavioral addicts often recognize that their actions are causing a problem, but as with any addiction, they find the behavior impossible to control. Behavior addiction can be socially and psychologically damaging, rivaling substance addiction in the ability to cause havoc in family structure. However, behavioral addictions are often overlooked, even though its markers are similar to those of substance addiction.

Many health care professionals believe that addiction in one area is indicative of addictive tendencies in general, and persons who have these tendencies are likely to exhibit addictive behavior in many areas of life. Thus, substance abuse and behavioral abuse often go hand-in-hand, and screening for one type of addiction should include screening for all types.

Risk Assessment Screen

A diagnosis of substance addiction is often fairly clear. However, behavioral addiction is a much harder diagnosis for a professional to make. Often, this type of addiction is overlooked even though it coexists with substance addiction.

Clinical psychologist James Slobodzien introduced a tool called behavior risk assessment screen (BRAS) for professionals to use when they suspect addictive behavior. This tool screens for addictive behavior in seven areas: substance intake (nicotine, alcohol, illicit drugs, caffeine), eating attitude, exercise patterns, sleep patterns, sexual practice, gambling practices, and risky behaviors (impulsive behaviors with negative consequences such as reckless driving and starting fires).

Each of the seven areas includes two or three statements read by the tested subject. The subject then decides which of the statements best describes his or her behavior. Each statement is then given a standardized weighted classification, and the number of points is totaled for a cumulative score called a prognostic assessment gauge score, which ranges from 0 to 100.

This score is further broken into twenty-point categories ranging from excellent (80–100), good (60–80), fair (40–60), poor (20–40), and guarded (0–20). These point categories characterize how well the subject is coping with addictive behavior. The final score represents a person’s overall psychological, social, and occupational function and is comparable to a global assessment of functioning score (part of the
Diagnostic and Statistical Manual of Mental Disorders
).

CAGE Assessment Tool

The CAGE assessment tool screens for alcohol abuse. However, because it attempts to identify addictive behaviors, this simple tool is used by many providers as a basis for any type of addiction, including behavioral addictions, by substituting the type of addictive behavior for the term drinking in the questions.

The screen consists of four questions: Have you felt the need to cut down on your drinking? Do you feel annoyed or angered by others’ criticism of your drinking? Have you ever felt guilty about your drinking? And do you need to drink soon after waking as an eye-opener?

In using this tool to screen for behavioral addiction, two additional questions have been suggested to form the acronym “CAGED”: Do you feel empty when you’re not (for example) eating or gambling? Does (for example) eating or gambling disrupt your life or are you neglecting parts of your life because of it? These two additional questions may help pinpoint and further define behavioral addiction. Addictive tendencies may be a concern if the person being screened answers “yes” to two or more of the questions.

Screening for Specific Behavior Addictions

The BRAS and CAGE or CAGED assessments can give an idea of whether a person has addictive tendencies, including both behavioral and substance addictive tendencies. However, each type of addictive behavior has specific, though similar, screening instruments to determine whether the screening subject has that specific behavior addiction. Some examples follow.

Gambling. The LIE/BET screening for gambling consists of two questions: Have you ever had to lie to people important to you about how much you gambled? Have you ever felt a need to bet more money? A “yes” answer to either question would indicate that a person should be evaluated further. The South Oaks gambling screen is more complex, with sixteen questions (and several subquestions) rating the behavior of the person being screened. The questions are answered with the terms not at all, less than once a week, or once a week or more. This screening tool asks questions about the amounts of money used in gambling, family or friends who gamble, and several more related to gambling behavior. Answers to these questions are then weighted and scored, with a score of 5 or more indicating problem behavior. Gamblers Anonymous also has a twenty-question screening tool; seven or more yes answers means the person is likely to be a compulsive gambler.

Sexual activity. The WASTE Time tool is a quick screening for sex addiction. This tool assesses functional indicators such as withdrawal, adverse consequences, inability to stop, tolerance or intensity, and escape, with time spent on sexual activity being the final element of the screen. Answering “yes” to even one of the screening questions indicates a possible problem; answering “yes” to two or more questions indicates a high probability of sex addiction. Another screening for sexual addiction is the sexual addiction screening test, which consists of forty-five questions. Answering “yes” to more than seven of the first twenty questions indicates a sexual addiction, while the rest of the questions are intended to help pinpoint the problem’s manifestations.

Eating disorders
. EAT-26 is a common screening tool to assess eating behavior addictions such as overeating, anorexia nervosa, or bulimia nervosa. The tool consists of personal-information questions that assess attitudes about ideal weight, with twenty-six yes/no questions, and six behavioral questions. Items are scored on a scale of 1 to 3; if the total score is above 20, further help may be needed. However, even a score of less than 19 may refer a person for further help if binging or purging behavior is indicated by the screening.

Internet use. The Internet addiction test may be used as a screening tool for Internet addiction. The test screens with twenty questions that are rated on a scale using the terms does not apply or rarely to always. Each question is scored, and a total score is assigned (between 0 and 100). These scores are broken into ranges of 0–19 (below average), 20–49 (average), 50–79 (above average), and 80–100 (significantly above average). A score of 80 or above is cause for referral for further help.

Work. The work addiction risk test consists of twenty-five questions pertaining to attitudes toward work and to related behaviors in particular and life in general. The person being screened answers each question on a scale of 1 to 4, with 1 representing “never true” and 4 representing “always true.” The numbers are then added into a total score, in which 25–54 represents “not work addicted,” 55–69 represents “mildly work addicted,” and 70–100 represents “highly work addicted.”

Bibliography

Crozier, Mary K., and Steven R. Sligar. “Behavioral Addiction Screening during the Vocational Evaluation Process.” Vocational Evaluation and Work Adjustment Association Journal 37 (2010): 45–57. Print.

Freimuth, Marilyn. “The ‘New Look’ in Addiction Assessment: Implications for Medical Education.” Annals of Behavioral Science and Medical Education 16.1 (2010): 30–34. Print.

Petry, Nancy M. Behavioral Addictions: DSM-5 and Beyond. New York: Oxford UP, 2016. Print.

Rosenberg, Kenneth Paul, and Laura Curtiss Feder. Behavioral Addictions: Criteria, Evidence, and Treatment. New York: Academic, 2014. Print.

Whitlock, Evelyn, et al. “Evaluating Primary Care Behavioral Counseling Interventions: An Evidence-Based Approach.” American Journal of Preventive Medicine 22.4 (2002): 267–84. Print.

In The Witch of Blackbird Pond, what does hiding the charter mean to the king?

King Charles granted Connecticut a charter.  This charter guaranteed "every right and privilege."  It also guaranteed their land and the laws that the citizens of Connecticut had established.

During a meeting with Governor Treat, the charter lay on "the table in plain sight."  As the evening came, the room grew dark.  Candles were lit, but the room became very warm.  It also was filled with smoke because of all the lit candles required to light...

King Charles granted Connecticut a charter.  This charter guaranteed "every right and privilege."  It also guaranteed their land and the laws that the citizens of Connecticut had established.

During a meeting with Governor Treat, the charter lay on "the table in plain sight."  As the evening came, the room grew dark.  Candles were lit, but the room became very warm.  It also was filled with smoke because of all the lit candles required to light the room.  To relieve the occupants of the room from the heat and smoke, "someone opened a window."  This caused a draft to come inside through the window and it "blew out the candles."  The candles were relit, but this task took time.  When the room was once again filled with the brightness of candlelight, it was discovered that the charter had vanished.  

When William came to see Matthew to tell the story of what had happened, he assured him that the charter was safely hidden.  Whoever took the charter had committed an act of "serious insubordination to the King."  This was an act of rebellion against the authority of the King of England.

What are tumor-suppressor genes? |

Discovery of Tumor-Suppressor Genes

The existence of genes playing critical roles in cell cycle regulation by inhibiting cell division was predicted by several lines of evidence. In vitro studies involving the fusion of normal and cancer cell lines were observed to result in suppression of the malignant phenotype, suggesting normal cells contained inhibitors with the ability to reprogram the abnormal growth behavior of the cancer cell lines. In addition, back in 1971, studies by Alfred Knudsen on inherited and noninherited forms of retinoblastoma, a childhood cancer associated with tumor formation in the eye, suggested the inactivation of recessive genes as a consequence of mutation, resulted in the loss of function of inhibitory gene products critical to cell division control. With the advent of molecular methods of genetic analysis, the gene whose inactivation is
responsible for retinoblastoma was identified and designated Rb.

Additional tumor-suppressor genes were identified by studies of DNA tumor viruses whose cancer-causing properties were found to result, in part, from the ability of specific viral gene products to inactivate host cell inhibitory gene products involved in cell cycle regulation. By inactivating these host cell proteins, the tumor virus removes the constraints on viral and cellular proliferation. The most important cellular gene product to be identified in this way is the p53 protein, named after its molecular weight. Genetic studies of human malignancies have implicated mutations in the p53
gene in up to 75 percent of tumors of diverse tissue origin, including an inherited disorder called Li-Fraumeni syndrome, which is associated with a higher risk for developing sarcomas, brain tumors, adrenal gland cancers, and leukemias. In addition, studies of other rare inherited malignancies have led to the identification of about thirty recessive tumor-suppressor genes whose inactivation contributes to oncogenic or cancer-causing cell proliferation. The accompanying table provides examples of the chromosomal locations for several tumor-suppressor genes. Included in the list are the BRCA1
and BRCA2 genes in breast cancer, the NF1 gene in neurofibromatosis, the p16 gene in melanoma, and the APC gene in colorectal carcinoma. Each of these genes has also been implicated in nonhereditary cancers. Three types of tumor-suppressor genes are generally recognized: genes controlling cell division, DNA repair, and cell death.

The Properties of Tumor-Suppressor Genes

Molecular analyses of the genetic and biochemical properties of tumor-suppressor genes have suggested some of these gene products play critical but distinct roles in regulating processes involved in cellular division and proliferation. The Rb gene product represents a prototype tumor-suppressor gene of this type. The Rb gene product normally blocks progression of the cell cycle and cell division by binding to transcription factors in its active form. In order for cell division to occur in response to growth factor stimulation, elements of the signal cascade inactivate Rb-mediated inhibition by a mechanism involving the addition of phosphate to the molecule, a reaction called phosphorylation. In cancer, loss of Rb function results as a consequence of mutation which removes the brakes on this form of normal inhibitory control; the cell division machinery proceeds without appropriate initiation by growth factors or other stimuli.

Like the Rb tumor-suppressor gene, most tumor-suppressor genes become active due to a loss of heterozygosity (LOH). Since chromosomes (and the genes residing within the chromosomes) are paired, a mutation in one gene of the pair is called heterozygosity. For Rb, a single gene mutation (the heterozygous condition for the trait encoded by the gene pair) is inherited as a recessive condition where no cancer results (since the infant has one normal gene and one mutated Rb gene). During development however, a random mutation can occur in the normal Rb gene. As soon as the second Rb gene mutates in a single cell, cancer can begin.

Tumor-suppressor genes are also found among the genes specifically involved in DNA repair. Whenever a cell divides the DNA must be duplicated, and errors in the duplication process must be repaired in order for the new cell to function properly. The protein products of DNA repair gene errors in duplicated DNA by proofreading the DNA sequence; however, if the DNA repair genes are mutated, errors will slip by and these mutations can create proteins which may activate oncogenes, or the mutations may create abnormal, mutated tumor-suppressor genes. For example, when DNA repair genes fail to repair DNA errors, some endometrial cancers and hereditary nonpolyposis colon cancer (HNPCC) can result (about 5 percent of all colon cancers).

If the cell’s DNA is damaged beyond repair by the DNA repair proteins, then the p53 tumor-suppressor gene is among the family of genes responsible for destroying the cell by causing cell death (also called “cell suicide” or “programmed cell death” or “apoptosis”). The p53 tumor-suppressor gene product is a DNA-binding protein with the ability to regulate the expression of other genes in response to genetic damage or other abnormal events occurring during cell cycle progression. In response to p53 activation, the cell will normally arrest the process of cell division (by indirectly blocking Rb inactivation). This cell cycle arrest may allow time for the cell machinery to repair genetic damage before proceeding further along the cell cycle; alternatively, if the damage is too great, the p53 gene product may initiate a process of apoptosis. The loss of p53 activity in the cell as a consequence of mutation results in genetic destabilization and the failure of cell death mechanisms to eliminate damaged cells from the body; both events appear to be critical to late-stage oncogenic mechanisms. Mutations of the p53 gene may be inherited (as in the Li-Fraumeni syndrome, LFS); however, mutations in p53 are also routinely found in many sporadic (noninherited) cancers (including lung, colon, breast, and other cancer types).

Impact and Applications

The discovery of tumor-suppressor genes has revealed the existence of inhibitory mechanisms critical to the regulation of cellular proliferation. Mutations that destroy the functional activities of these gene products cause the loss of growth control characteristic of cancer cells. Taken together, research on the patterns of oncogene activation and the loss of tumor-suppressor gene function in many types of human malignancy suggest a general model of oncogenesis. Molecular analyses of many tumors show multiple genetic alterations involving both oncogenes and tumor-suppressor genes, suggesting that oncogenesis (development of cancer) requires unregulated stimulation of cellular proliferation pathways along with a loss of inhibitory activities that operate at cell cycle checkpoints.

Some tumor-suppressor gene mutations are inherited and, in rare cases, testing for these gene mutations (which have been found often enough in the general population, like BRCA 1 and BRCA 2) may be helpful to determine which people are at higher risk for certain cancers. Genetic testing for families at risk requires careful screening and counseling and might allow surgical intervention, lifestyle changes, or more frequent cancer screening steps to minimize the individual’s familial cancer risk.

Genetic tests for oncogenes and tumor-suppressor genes have become commonplace in cancer diagnosis and treatment. Some genetic tests have been shown to help diagnose the type of cancer, guide cancer treatment, predict survival for patients with cancer, and sometimes to produce novel therapies for cancer patients.

With respect to clinical applications, restoration of p53 tumor-suppressor gene function by gene therapy appears to result in tumor regression in some experimental systems; however, much more work needs to be done in this area to achieve clinical relevance. More important, research on the mechanism of action of standard chemotherapeutic drugs suggests that cytotoxicity may be caused by p53-induced cell death; the absence of functional p53 in many tumors may account for their resistance to chemotherapy. Promising research is investigating new ways to elicit cell death in tumor cells lacking functional p53 gene product in response to chemotherapy. The clinical significance of activating these p53-independent cell death mechanisms may be extraordinary.

Key Terms




cell cycle


:

a highly regulated series of events critical to the initiation and control of cell division processes





oncogenes


:

mutated or improperly expressed genes known to cause cancer; the normal form of an oncogene is called a proto-oncogene, which is usually involved in regulating the cell cycle; however, activating or “turning on” the proto-oncogene (through mutation or improper expression) results in cancer




p53 gene

:

a tumor-suppressor gene implicated in many types of cancer




Rb gene

:

a tumor-suppressor gene, when inactivated, is associated with several cancers including the formation of a rare and lethal eye tumor (retinoblastoma) in infants





Bibliography

DeCaprio, J. A. “How the Rb Tumor-Suppressor Structure and Function Was Revealed by the Study of Adenovirus and SV40.” Virology 384.2 (2009): 274–84. Print.

Ehrlich, Melanie, ed. DNA Alterations in Cancer: Genetic and Epigenetic Changes. Natick: Eaton, 2000. Print.

Fearon, Eric, and Bert Vogelstein. “Tumor Suppressor Gene Defects in Human Cancer.” Cancer Medicine. Ed. Robert C. Bast, Jr., et al. 5th ed. Atlanta: American Cancer Society, 2000. Print.

Fisher, David E., ed. Tumor Suppressor Genes in Human Cancer. Totowa: Humana, 2001. Print.

Gunduz, Mehmet, and Esra Gunduz. Tumor Suppressor Genes: Functions, Regulation and Health Effects. New York: Nova Biomedical, 2013. Print.

Habib, Nagy A. Cancer Gene Therapy: Past Achievements and Future Challenges. New York: Kluwer Academic/Plenum, 2000. Print.

Iglehart, J. Dirk, and Daniel P. Silver. “Synthetic Lethality: A New Direction in Cancer-Drug Development.” New England Journal of Medicine 361.2 (2009): 189–91. Print.

Lattime, Edmund C., and Stanton L. Gerson, eds. Gene Therapy of Cancer: Translational Approaches from Preclinical Studies to Clinical Implementation. 3rd ed. San Diego: Academic, 2014. Print.

Maruta, Hiroshi, ed. Tumor-Suppressing Viruses, Genes, and Drugs: Innovative Cancer Therapy Approaches. San Diego: Academic, 2002. Print.

Nguyen, Susan D. Tumor Suppressors. New York: Nova Science, 2011. Print.

Oliff, Alan, et al. “New Molecular Targets for Cancer Therapy.” Scientific American 275 (September, 1996). Print.

Ruddon, Raymond. Cancer Biology. 3rd ed. New York: Oxford UP, 1995. Print.

Compare Shelley's description of the setting to Victor's mood.

After the murder of William and the execution of Justine, Victor's family goes to the valley of Chamounix in an attempt to restore their spirits and find some happiness again.  Victor uses the word "sublime" many times to describe the beauty of the natural setting and its effect on him.  Such a word implies a great deal more than physical beauty; it implies that the nature Victor sees is inspiring, even transcendent.  These sights urge...

After the murder of William and the execution of Justine, Victor's family goes to the valley of Chamounix in an attempt to restore their spirits and find some happiness again.  Victor uses the word "sublime" many times to describe the beauty of the natural setting and its effect on him.  Such a word implies a great deal more than physical beauty; it implies that the nature Victor sees is inspiring, even transcendent.  These sights urge personal growth, perhaps even personal change, because they are so affective.  He says that

"These sublime and magnificent scenes afforded me the greatest consolation that I was capable of receiving.  The elevated me from all littleness of feeling; and although they did not remove my grief, they subdued and tranquillized [sic] it."  

Although he, at times, "indulged in the misery of reflection," Victor cannot help but be affected and changed by the natural beauty he sees around him in this place.  He marked the mountains, the river winding through the valley, the sound of the waterfalls, and their splendor begins to heal him.  The more time he spends in nature, reveling in its sublimity, the better he feels, and he knows that this was what his father intended when he proposed the journey.  

What is acid reflux disease?

Causes and Symptoms

Approximately one-third of Americans experience heartburn at least once a month, and 10 percent experience the sensation daily. Heartburn reportedly affects sufferers during the day and at night, impacting their job performance as well as their sleep. Heartburn is the major symptom of acid reflux

disease, also called gastroesophageal reflux disease (GERD). A burning sensation radiating up through the middle of the chest

behind the sternum (breastbone) characterizes heartburn, which can be aggravated by a variety of foods; alcohol; emotions such as anger, fear, or stress; and even particular positions such as reclining, lifting, or bending forward. Abdominal exercises, girdles, and tight belts can increase abdominal pressure and trigger reflux. Many women experience heartburn
during pregnancy, especially in the later stages. Overweight people and smokers are also commonly affected.

Common foods and beverages implicated in acid reflux disease include coffee, tea, cocoa, cola drinks, mints, chocolate, fried and fatty foods, onions, garlic, citrus fruits, tomato products, and spicy foods. This list is not exhaustive, and certain people may be troubled by substances not included. Medications can exacerbate heartburn and reflux, including, but not limited to, oral contraceptives; aspirin; medications used to treat asthma, rheumatoid arthritis, and osteoporosis; antidepressants; and tranquilizers. Additionally, medical conditions such as asthma, diabetes, peptic ulcers, and some cancers may contribute to acid reflux disease, as can treatments such as chemotherapy or narcotic use for pain management.

The lower esophageal sphincter (LES), which connects the esophagus
to the stomach, acts as a barrier to protect the esophagus from the backflow of acid from the stomach. Normally, it works like a dam, opening to allow food to pass into the stomach and closing to prevent food and acid from flowing back into the esophagus. If the sphincter weakens or relaxes, the contents of the stomach flow up into the esophagus. The reason for this occurrence is uncertain, but it is known that sphincter function can be impaired by diet, medications, and nervous system factors. Other factors that can also contribute to acid reflux disease include impaired stomach motility or an inability of the stomach muscles to contract normally, resulting in a delayed emptying of the contents. The acid remains at the top of the stomach near the LES rather than moving downward, creating pressure and reflux. Failure of contractions to clear the acid or a shortage of
saliva to neutralize the acid may also contribute to heartburn.

Hiatal hernia,
a condition in which a portion of the stomach protrudes into the chest cavity through an opening (hiatus) in the diaphragm (the muscle separating the chest and abdomen), exists to some degree in about 30 percent of Americans. In cases of hiatal hernias so large that they risk strangulation (becoming twisted and cutting off blood supply), complicated by severe GERD or esophagitis, surgery may be performed. Otherwise, medication in the form of a histamine blocker, which suppresses the secretion of stomach acids, is used.

Treatment and Therapy

Medical tests often used to evaluate the presence and severity of acid reflux disease include barium studies and upper endoscopy. Other tests performed less frequently include pH monitoring (to measure reflux over a twenty-four-hour period), the Bernstein test, and esophageal manometry. In the Bernstein test, which is used to evaluate the cause of chest pain after heart problems have been ruled out, saline and diluted hydrochloric acid are infused into the esophagus. If this reproduces the patient’s symptoms, it can be inferred that reflux is the cause. Esophageal manometry measures pressure in the esophagus and LES.

Counseling patients to modify their diet and lifestyle is the basic treatment for reflux symptoms. Generally, patients should eat smaller meals more often and more slowly, avoiding spicy foods and those that increase acid production. They should not have bedtime snacks. Patients should relax both while eating and between meals. They should remain upright after eating and should not bend, strain, or lift for the following three hours. Those who are overweight should lose excess pounds, and patients should not smoke or chew gum. They should exercise on an empty stomach and avoid tight, constricting clothing, which may put pressure on the stomach. Patients with GERD should elevate the head of their beds by placing blocks under the beds’ legs.

Over-the-counter antacids (Tums, Rolaids, and Mylanta, for example) can be effective in reducing or neutralizing acid in mild cases of heartburn. In chronic cases, however, histamine blockers may be prescribed. These medications act directly on the acid-secreting cells in the stomach to stop them from producing hydrochloric acid that can wash into the esophagus. Several of these medications (Tagamet, Zantac, and Pepcid) are available over the counter. Prokinetics or gastrokinetics are a group of medications that increase the speed at which the stomach empties food, acid, and fluids. In severe cases of GERD, they may be used instead of histamine blockers. Another class of medication is the proton-pump inhibitor or acid-pump inhibitor, which suppresses acid secretion in the stomach by inactivating the enzyme responsible for acid release in the stomach. These medications include Prevacid, Aciphex, Protonix, Nexium, and Prilosec (the latter is available over the counter). Additionally, chamomile, ginger, licorice, catnip, papaya, pineapple, marshmallow root, and fennel have all
been said to aid in digestion.

Approximately 95 percent of GERD cases are controlled by medication; the remainder require surgery (fundoplication) to tighten the LES. Another technique is radiofrequency ablation, which applies controlled radiofrequency energy to the LES and upper part of the stomach, causing the lining to expand slightly as the valve tightens. The Bard endoscopic suturing system places stitches on either side of the sphincter; as the physician ties the sutures together, the valve tightens.

Bibliography:

"GERD." MedlinePlus, Apr. 8, 2013.

Lasalandra, Michael, and Lawrence S. Friedman. The Sensitive Gut. New York: Fireside, 2001.

Rosenthal, M. Sara. Fifty Ways to Relieve Heartburn, Reflux, and Ulcers. Chicago: Contemporary Books, 2001.

Sachar, David B., Jerome D. Waye, and Blair S. Lewis, eds. Pocket Guide to Gastroenterology. Baltimore: Williams & Wilkins, 1991.

Udall, Kate Gilbert. Managing Acid Reflux. Orem, Utah: Woodland, 2007.

Wood, Debra, and Daus Mahnke. "Heartburn—Overview." Health Library, Sept. 27, 2012.

What is sex addiction? |

Causes

The causes of sex addiction are not known. Nevertheless, as with substance addictions, most research focuses on the structures of the brain’s mesolimbic reward system and the neurotransmitter (chemical messenger) dopamine . Most researchers believe that the mesolimbic reward system evolved to sustain behaviors that are necessary for survival and reproduction—namely, the pursuit of food, water, and sex.

Normal sexual arousal and orgasm involve excitation in the mesolimbic reward system. In sex addiction, repeated sexual behavior is hypothesized to result in excessive stimulation of dopamine pathways in structures of the mesolimbic reward system (for example, the striatum), thereby causing changes at the cellular level (fewer dopamine receptors) that lead to even greater desire and cravings to engage in the behavior.

As in substance addictions, classical conditioning appears to play a role in the development and maintenance of many sexually addictive behaviors. Stimuli that are present when an addict engages in the problem behavior, such as a computer that the person uses to view pornography or a street where the person has often visited a strip club, can become powerful triggers for the desire to engage in the addictive behavior.

Risk Factors

Men are at higher risk than women for sex addiction. Although high-quality epidemiological data are lacking, the substantial majority (80 percent or more) of sex addicts addressed in published work are male. Access to numerous sexual partners also may be a risk factor. Thus, men who are famous or socially powerful may be at especially heightened risk for sex addiction.

In 2010, tremendous media attention focused on the alleged sex addiction of golf superstar Tiger Woods, who was reportedly treated for the condition. In 2011, Anthony Weiner resigned from the US House of Representatives because of his alleged involvement in a sexting scandal. Although both Woods and Weiner and numerous other high-profile persons with “excessive” sexual activity were labeled as “sex addicts” by much of the popular media, it is not known whether either men met any formal or informal criteria for sex addiction.

Some experts have suggested that childhood sexual abuse may play an important role in the development of sex addiction. Nevertheless, available research suggests that childhood sexual abuse is a nonspecific risk factor for a broad range of mental health difficulties during adulthood rather than a specific risk factor for sex addiction.

Although pornography viewing and masturbation are common manifestations of sex addiction, these behaviors are common among adult men, and the vast majority of these men will never develop behaviors that are compulsive or otherwise problematic. Thus, masturbation and pornography are not considered risk factors for sex addiction.

Some clinicians believe rates of sex addiction have increased in recent years because of the Internet. They argue that the Internet has made pornography, and connection with casual sex partners and prostitutes, far more accessible, anonymous, and affordable than ever before. This claim is plausible, but there is no firm data to support or refute it.

Symptoms

The manifestations of sex addiction are diverse. Nevertheless, all manifestations involve a preoccupation with sexual thoughts, fantasies, or urges and sexual activity that is excessive in frequency or duration. The behavior is pursued despite obvious costs and consequences, such as loss of a job or relationship or getting a sexually transmitted disease. Many sex addicts have repeatedly attempted to discontinue or curb their behavior unsuccessfully.

There is controversy concerning whether sex addicts exhibit tolerance and withdrawal. In support of the view that tolerance develops, some have observed that many sex addicts take greater risks over time and engage in increasingly extreme or unusual sex acts. Similarly, some argue that withdrawal is evident in the frustration and anger sex addicts experience when they cannot engage in the desired sexual behaviors.

Many clinicians have reported that sex addicts use sexual behavior as a way to cope with unpleasant emotions; this possibility needs to be examined in systematic research. Data are limited, but preliminary information suggests that sex addiction is highly comorbid (overlapping), not only with substance addictions but also with anxiety and mood disorders.

Sex addiction may manifest differently in women than in men. Rather than focusing on fantasies and behaviors associated with sexual gratification, as do most men with sex addiction, some women who self-identify as sex addicts appear to experience an ongoing series of intense romantic attachments toward new partners. The romantic attachments may develop toward inappropriate persons (such as a coworker or boss) and despite possible negative consequences (such as the loss of one’s marriage). Although no systematic data are available, there have been occasional reports of men who experience such a series of attachments to many partners over time. Some authors refer to this ongoing pattern of new romantic attachments as love addiction.

Screening and Diagnosis

As noted, sex addiction is not recognized as a formal mental health diagnosis. However, because of the need for a diagnosis for sexual behavior (intercourse or masturbation) that is excessive in frequency or duration and causes subjective distress or impairment in social or occupational functioning, a related diagnosis of hypersexual disorder was considered for inclusion in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) but later rejected.

Hypersexual disorder has a narrower focus than does sex addiction. Whereas the former refers only to “normal” sexual behaviors that are habitual and cause distress or impairment, sex addiction refers either to such normal sexual behaviors or to deviant sexual behaviors (such as exhibitionism and fetishes) that are habitual and cause distress or impairment.

A clinician who suspects sex addiction should conduct a thorough interview, inquiring about the person’s sexual behaviors, urges, and fantasies and their frequency, duration, and consequences. Clinicians also may screen for sex addiction using various checklists and questionnaires.

Treatment and Therapy

Little research has been conducted on the efficacy of treatments for sex addiction. However, most treatment approaches for sex addiction parallel effective treatments for substance addictions. These approaches include behavioral therapy and cognitive-behavioral therapy. Such treatments teach addicts how to recognize and avoid stimuli that increase the risk of engaging in sexually inappropriate behavior. Such stimuli generally include people, places, and Internet sites associated with the addict’s previous maladaptive sexual behavior.

Because many sex addicts engage in sexually inappropriate behaviors in response to negative emotions, sex addicts may be taught skills that enable them to cope with negative feelings more adaptively and to identify situations that may trigger unpleasant emotions, such as anger or feelings of loneliness. Cognitive-behavioral therapy interventions also seek to identify and correct erroneous beliefs (for example, “I will be miserable if I cannot have sex when I have the urge to do so”) that the addict maintains about sex or romantic relationships.

In addition to embracing traditional psychotherapy, many clinicians and recovering sex addicts believe twelve-step programs (support groups modeled after Alcoholics Anonymous, or AA) are helpful to recovering sex addicts. Note, however, that whereas AA promotes complete abstinence from alcohol, twelve-step groups for sex addicts promote responsible sexual behavior rather than abstinence. Inpatient treatment programs for sex addiction exist and are typically used when outpatient treatments fail to curb life-threatening behaviors, such as frequent unprotected sex with strangers.

In extreme cases in which a sex addict’s behavior is illegal or harmful to others (such as with exhibitionism), antiandrogen medications (including Depo-Provera, or depot medroxyprogesterone acetate) are sometimes prescribed to reduce the person’s sex drive. Nevertheless, controlled studies to ascertain whether these medications are effective for sex addiction are lacking.

Prevention

No research has been conducted on the prevention of sex addiction.

Bibliography

Carnes, Patrick J. Don’t Call It Love: Recovery from Sexual Addiction. New York: Bantam, 1991. Print.

Cooper, Alvin. “Sexuality and the Internet: Surfing into the New Millennium.” Cyberpsychology and Behavior 1.2 (1998): 187–93. Print.

Kafka, Martin P. “Hypersexual Disorder: A Proposed Diagnosis for DSM-V.” Archives of Sexual Behavior 39.2 (2010): 377–400. Print.

Reid, Rory C., and Martin P. Kafka. “Controversies about Hypersexual Disorder and the DSM-5.” Current Sexual Health Reports 6.4 (2014): 259–64. PDF file.

Rosenberg, Kenneth Paul, Patrick Carnes, and Suzanne O'Connor. “Evaluation and Treatment of Sex Addiction.” Journal of Sex & Marital Therapy 40.2 (2014): 77–91. Academic Search Complete. Web. 28 Oct. 2015.