There are some people who are always sick while others are okay. People become sick due to pathogens. ‘pathogen’ means disease, a pathogen is an agent that produces a disease. it means suffering; it is an infectious agent, or germ, that causes disease or illness to the living organ. Many of these pathogens can make us sick and some can cause death. for pathogens to be successful and cause disease they must be able to overcome certain challenges to survive. they must; (1) find a host, (2) Attach and colonise, (3) Invade and evade the host’s defenses, which causes damage to the host, and (4) be able to survive outside of the host.

The body contains many natural defenses against some of the common pathogens in the form of the human immune system and by some ‘helpful’ bacteria present in the human body’s normal flora. however, if the immune system or ‘good’ bacteria is damaged in any way (such as by chemotherapy, human immunodeficiency virus (HIV), or antibiotics being taken to kill other pathogens), pathogenic bacteria that were being held at bay can cause harm to the body. such cases are called opportunistic infections.

Groups of pathogens or germs;there are five main groups of pathogens; viruses, bacteria, fungi, protozoa (which include the malaria parasite) and intestinal parasites (such as flatworms and roundworms). .

Viruses: Consist of genetic materials surrounded by a protective coat of protein. they are capable of latching onto cells and getting inside them. The cells of the mucous membranes, such as those lining the respiratory passages that we breathe through, are particularly open to virus attacks because they are not covered by protective skin.

Bacteria: are organisms made up of just one cell. they are capable of multiplying by themselves, as they have the power to divide. Their shapes vary, and doctors use these characteristics to separate them into groups. Bacteria exist everywhere, inside and on our bodies. most of them are completely harmless, and some of them are very useful. But some bacteria can cause diseases, either because they end up in the wrong place in the body, or simply designed to invade us.

Fungi: Fungi are a group of organisms and micro-organisms that are classified within their own kingdom, the fungal kingdom, as they are neither plant nor animal. Fungi draw their nutrition from decaying organic matter, living plants and even animals.

Protozoa: The protozoa are one-celled animals and the smallest of all animals. most of them can only be seen under a microscope. they breathe, move, and reproduce like other animals. they live in water or at least where it is damp. they can be free-living or parasitic in nature. While protozoa can be an important source of food for animals like snails, they can also cause serious infections in humans. Protozoa can be transmitted to the body by eating contaminated food or water, person-to-person contact, or through the bite of an insect like a mosquito or fly. While many protozoan infections are more common in the tropics and subtropics, they can also affect people in temperate zones as well, a common example of protozoa is malaria and some sexually transmitted  infections.

Intestinal worms: Intestinal worms are living organisms with many cells such as; tapeworms, pinworms, and roundworms. Risk factors for intestinal worms include; living in or visiting an area known to have parasites , international travel, poor sanitation (for both food and water), poor hygiene, age — children are more likely to get infected  and HIV or AIDS. Symptoms of parasites include; diarrhea, nausea or vomiting, gas or bloating, dysentery (loose stools containing blood and mucus), rash or itching around the rectum or vulva, stomach pain or tenderness, feeling tired, weight loss and passing a worm in your stool.

Nutrition in viral infection:a stomach virus inflammation of the stomach and other digestive organs, symptoms of stomach viruses include diarrhea, vomiting, pain, fever and abdominal pain. Stomach viruses may be triggered by contaminated water, food or contact with feces from an infected person. Home remedies for treating stomach viruses include preventing dehydration, eating certain foods and limiting physical activity.Drink substantial amounts of fluids, diarrhea and vomiting that may occur, patients with stomach viruses frequently run the risk of becoming dehydrated. Sucking on ice chips and drinking small sips of water helps with dehydration symptoms that originate from diarrhea and vomiting. Clear sodas and other beverages such as non-caffeinated sports drinks and chicken broth also help restore the balance of salts in the human body and prevent dehydration.Stomach virus patients should avoid eating solid food as this worsens the condition. Examples of these foods include greasy foods, dairy products, orange juice, tea, alcohol and coffee. Instead, eat bland foods such as saltine crackers, bananas, rice, gelatin and dry toast. These foods help settle the stomach and promote digestion.Limit physical activity at home. Symptoms of the stomach virus often include fatigue, dizziness and weakness. Resting helps the stomach to settle and ease symptoms that can result from sudden movement or activity. Rest as much as possible until a full recovery is made. Practice preventive measures. most infectious bacteria and viruses are transmitted by unwashed hands. Washing hands before handling food and after using the toilet is the best way to prevent stomach viruses. In addition, avoid contaminated raw meats, eggs and other foods to reduce the spread of stomach viruses. it is also recommended to thoroughly cook food to the proper temperature.

Nutrition in bacterial infections:Bacteria can cause multiple types of infections and illnesses, including many stomach and bowel problems. Preventing bacterial infections can have a great effect on your health. Wash your hands often, clean fruits and vegetables before you eat them, and make sure your food is fresh, prepared correctly, and cooked thoroughly. Fighting bacterial growth and spread come down to keeping things clean. But no matter how clean you keep yourself and your surroundings you will still have to deal with bacteria as you live in the world and not a bubble. Treatments for bacterial infections or bacterial illness may depend on what type of bacteria you have been infected with. there are both internal and external bacteria and this will affect the treatment.

Natural Cures for Bacterial infections:Some types and amounts of stomach bacteria are good for stomach and colon health. Overgrowth and bad types of bacteria can cause many illnesses. Simple and natural remedies with minimal side effects can be administered at home to treat and prevent bacterial infections, but it is important to note that these methods do not substitute for professional health care.Drinking plenty of fluids, such as water, broths, and juices, can play a major role in maintaining overall health. Fluids can help flush bacteria from the body via urine. Fluids also help to improve circulation of blood in the body, thereby improving immunity and the body’s ability to fight infections. Avoid drinking apple or pear juices, caffeine and alcohol when suffering from diarrhea, which is commonly associated with bacterial gastrointestinal infections. Consumption of semi-solid foods and low-fiber foods and avoiding dairy products can also help improve bowel movements and diarrhea. Drinking at least one or two glasses of cranberry or blueberry juice per day is known to prevent colonisation of the bacteria. Drinking large amounts of water and eating a cup of pineapple can also help treat urinary tract infections.

for this reason, the Minnesota Daily’s website cannot offer great legacy support for IE 6 / 7 users at this time. to get the best possible experience on our website, we strongly recommend that you upgrade to a newer version or another more modern browser. such as:

Internet Explorer 8+, Mozilla Firefox 3+, Google Chrome 2.0+, Apple Safari 3+, Opera 9.5+

to continue to the website anyway (not recommended), you may click here. If cookies are enabled in your browser, the website will remember this preference for a while.

If you aren’t using Internet Explorer 6 / 7 but were taken here anyway, or have any other complaints, please contact the Online Department.

the Minnesota Daily 2221 University Ave SE. Suite 450, Minneapolis, MN 55414 (612) 627-4080

Zimmerman held pending arraignment

SANFORD, Fla., April 12 (UPI) — A Florida judge Thursday ordered the neighborhood watch volunteer who killed unarmed Florida teenager Trayvon Martin to remain jailed on murder charges.

Seminole County Circuit Judge mark E. Herr ordered George Zimmerman, 28, held pending a bond hearing and formal arraignment on second-degree murder charges may 29 before Judge Jessica J. Recksiedler.

No plea was entered during Thursday’s brief teleconference hearing. Zimmerman answered, “Yes, sir,” to acknowledge he understood the charges.

Both defense attorney mark O’Mara and special prosecutor Angela Corey agreed records in the case should be sealed.

Zimmerman has admitted shooting and killing Martin, 17, Feb. 26 as the teen walked through a gated Sanford neighborhood. the shooting sparked outrage in the black community and police initially declined to file charges, citing Florida’s Stand Your Ground law.

Zimmerman, who is a white Hispanic, surrendered to police Wednesday.

Earlier Thursday, Martin’s mother said she believes the shooting “was an accident.”

Moscow terrorist group convicted

MOSCOW, April 12 (UPI) — Nine members of a Moscow terrorist group were convicted Thursday of setting off explosives and committing acts of arson.

The defendants, all age 16 to 20 and members of the Autonomous Combat Terrorist Organization, were found guilty in Moscow City Court of setting a kiosk on fire, igniting a cafe and a police station, throwing Molotov cocktails at a house and other similar crimes. the four-month trial was open to the press.

The group is regarded by the government as an extremist organization and was formerly affiliated with a since-banned organization noted for its nationalistic and anti-immigrant leanings, the news service ITAR-Tass reported Thursday.

At the trial, the prosecutor asserted the defendants’ actions were terrorist in nature, and after the conviction recommended leader Ivan Astashin be sentenced to 15 years in prison for crimes including terrorism, illegal explosives and inciting ethnic hate. the defense attorney argued the activities were merely acts of hooliganism.

Amid scandal, China hails corruption fight

BEIJING, April 12 (UPI) — China’s official state-run media is hailing the government’s crackdown on corruption as details of wealth amassed by deposed party official Bo Xilai emerged.

Bo’s family reportedly garnered huge wealth and influence while he was an influential member of the Chinese Communist Party Politburo from Chongqing. the local party boss had ambitions to rise to the nine-member Politburo Standing Committee, which effectively runs China, before his abrupt fall in March, the new York Times said.

Apple Daily, a Hong Kong newspaper, Thursday reported Bo’s older brother, Bo Xiyong, under an assumed name, for nine years was executive director and deputy general manager of a state-owned company that controlled a major Chinese bank and other lucrative businesses.

Chinese media this week began attempting to address the belief that nepotism is common among senior party members with relatives often getting high-paying jobs for family members at state-owned companies, the Times said.

Bo was suspended from the 25-member Politburo and party leaders said his wife was under investigation in the November death of British businessman Neil Heywood, who was found dead in Chongqing — the city-state formally run by Bo’s political machine.

Canadian troops get malaria drug U.S. quit

OTTAWA, April 12 (UPI) — Some Canadian veterans are questioning why troops are still being given an anti-malarial drug the U.S. military abandoned because of potential mental illness.

The drug marketed as Lariam is known generically as mefloquine and was dropped by U.S. forces in 2009 after a U.S. defense memo warned of potentially serious side effects, the Canadian Broadcasting Corp. reported.

“Mefloquine may cause psychiatric symptoms … ranging from anxiety, paranoia and depression to hallucinations and psychotic behavior … long after mefloquine has been stopped,” the memo said.

Regardless, Canada still gives its soldiers the drug in malaria-prone regions around the world based on advice from the Public Health Agency of Canada, which maintains the drug is “generally well tolerated,” the report said.

Retired Cpl. Donald Hookey of Newfoundland told the broadcaster he and his family see differences in him six years after he served in Afghanistan and he’s no longer convinced the nightmares and rage are solely because of post-traumatic stress disorder.

“I don’t think that I can honestly say that I’ve felt normal since I’ve been back,” he said.

Poll: Support for Afghan mission hits low

WASHINGTON, April 12 (UPI) — Only 30 percent of U.S. residents now believe the country should be fighting in Afghanistan, a poll released Thursday indicated.

The ABC News/Washington Post poll found that 66 percent of respondents oppose the war. Support for the effort is at its lowest level ever and has dropped below the lowest point in support for the Iraq war.

While Republicans remain far more supportive of the Afghanistan mission than Democrats and independents, only 44 percent said they now believe the war is worth fighting. That is a low point while support among the other groups is a few points higher than their record lows.

Attitudes toward the mission have often turned sharply because of external events. the Afghanistan mission was almost as unpopular a year ago and then support increased sharply after the killing of Osama bin Laden.

Langer Research Associates interviewed 1,003 adults by telephone last Thursday to Sunday. the margin of error is 4 points for the full sample.

Lori Thicke had an epiphany in Thange in eastern Kenya when she saw Aids orphans playing in front of posters with advice on Aids prevention. “The posters carried excellent advice, but they were in English, a language that people didn’t understand,” she said.

What was the use of this information provided by well-meaning NGOs, she wondered, if the people they were trying to reach could not read English. “People are delivering aid every day in Africa in English, French and Portuguese,” said Thicke. “That is fine for the educated elite, but they don’t need aid. It is the parents among the poor who need the information on symptoms of malaria.”

She saw the fatal effects of the language gap in India too, where mothers could have saved their children from dying from diarrhoea if they had followed the simple advice on health brochures and leaflets.

Thicke, a Canadian who came to Paris to write the great Canadian novel but founded a translation company instead, had pinpointed a glaring but little-noticed paradox in the information revolution. thanks to the internet and mobile phones, knowledge and information is disseminated far and wide and at speed. but that knowledge is wasted unless understood by those who need it most.

Translators without Borders was founded by Thicke and Ros Smith-Thomas in 1993 after Médecins sans Frontières, the medical NGO, asked her company, Lexcelera, to work on a translation project. She asked if they needed translation often, and if giving them the words for free would be like a donation. They said yes to both questions, and TWB was born. but until that moment in Kenya two years ago, the group dealt mostly with European languages. now Thicke is determined to bridge what she calls the “language last mile” in the developing world.

One of the group’s current projects is to teach sex workers in the Kibera slum of Nairobi, Kenya, to translate material in English on sexually transmitted diseases into languages such as Swahili, Luo and Kikuyu. The project started last week, with Simon Andriesen, a specialist on medical translation who is on the TWB board. He will teach about 125 women from Kibera, who speak different languages, to translate four-page brochures in English into the different Kenyan languages.

“He is teaching them translation skills so they can reach their own people,” said Thicke. “All the girls from Kibera represent different languages. They have been recommended to us by a health NGO and their job is to pass on information to other girls. we want to provide brochures in a language that can be understood so it doesn’t get thrown away.”

Paul Warambo, a recent masters graduate in the Kiswahili language living in Nairobi said: “The health translators training has come at a time when the country urgently needs translators in every sector, but especially in the health sector where little information is available in languages that can be understood by the majority of Kenyans.”

TWB is working on an even more ambitious project with Wikipedia. The aim is to take Wikipedia entries on the most important health topics, turn them into simple English and then translate them into as many languages as possible. The articles will then be accessible for free on mobile phones through new agreements betweek Wikimedia, which runs Wikipedia, and telecoms operators. A number of Wikipedia articles covering dengue fever, Aids, malaria, cholera and tuberculosis are awaiting translation from TWB’s army of volunteers.

The group has about 2,000 translators, who have passed its translation tests. Indian languages are well served but Africa is a big gap, with only about 15 of TWB’s translators able to deal with African languages. Africa has more than 2,000 different languages, such as Amharic, Swahili and Berber, spread across six major language families. Nigeria alone has more than 500 tongues spoken within its borders.

Until the 2010 Haiti earthquake, TWB had limited reach. but the crisis revealed not only the need for translations from thousands of aid groups that need humanitarian translations but also a critical mass of translators willing to help.

So the group created an online platform to bring the two communities together. last year, ProZ.com, the world’s largest translator organisation, created an automated translation centre for TWB so it could broaden its reach. Approved NGOs can now post translation projects such as field reports, treatment protocols and websites. Alerts then go out to the translators in those language pairs. those who are interested in the work of that particular NGO will take on a project, translate it, and return it to the platform for delivery. most of the projects are picked up within 15 minutes.

Translators without Borders can easily handle projects for 100 non-profits at a time, but as its volunteer community grows, so does its capacity. Over the years, it has donated almost $3m in translation services, which means that money went towards medical supplies, vaccines, rehydration kits and more.

“We are working to build a world where knowledge doesn’t have borders,” Thicke said. “With technology, and cellphone penetration in Africa, we have the potential to spread knowledge, but no one is talking about how people are getting information even if they are connected. People die not just of disease but from a lack of knowledge on how to avoid getting sick.”

An official in the Ministry of Health said yesterday that the one case of malaria reported in Exuma on Monday may have been contracted on the island.

Deputy Chief Medical Officer Dr. Delon Brennen said according to the information he received, the U.S. traveler who contracted the disease did so on the island because he did not visit any endemic country before visiting the Bahamas. Asked if there were any more people who had contracted the disease, Brennen said, “We don’t know yet. No one else has reported any symptoms. “It is very weird for one person to contract malaria. you have to have a source case somewhere.” Brennen said if a source case is not found the ministry would be a little more skeptical about if it was contracted on the island. According to Brennen, the person was staying in the George Town area, the same location previous victims contracted malaria in 2008 and 2006. “I don’t think the area in particular is the issue…the issue is…you having people who come into the area who have contracted malaria from some endemic country,”he said. the Nassau Guardian understands that government officials and hotel industry officials will meet today to discuss the recent case. Brennen noted that fogging has increased on the island. In 2006 four cases of malaria were recorded in the George Town area. all four of those cases were treated and the victims recovered, officials reported. On Monday, the Ministry of Health released a press statement on the latest case, noting that a team was mobilized to investigate. Brennen pointed out that unlike dengue fever, malaria could be treated. Malaria is not endemic in the Bahamas, but sporadic cases are encountered from time to time, the release noted. it is transmitted by the bite of the female anopheles mosquitoes.

UNIVERSITY PARK – In its fight against an intruding virus, an enzyme in our immune system may sense certain types of viral RNA pairs, according to scientists. The key lies in a virus’s RNA — a long molecular chain often used to make proteins — and how it regulates an enzyme called protein kinase R (PKR), according to researchers from Penn State, the University of Connecticut and the University of Beijing. “PKR plays an important role in the human immune system,” said Laurie Heinicke, graduate student of chemistry and first author for the paper. “It is activated by long stretches of double-stranded RNA. As a part of our built-in immune response, PKR can recognize viral double-stranded RNAs and inhibit their production.” Viral RNA enters human cells when attacking viruses inject their genetic material into the cells and force them to manufacture future generations of viruses. By latching on to specific sites on viral RNA, PKR can interrupt this process. or, according to Heinicke, “once activated by certain RNAs, PKR stops protein synthesis in the infected cell and ultimately causes cell death.” One way for this to happen is for the viral RNA to first form linked pairs called dimers. These RNA dimers then allow separate sets of PKR to bind with themselves, also forming dimers, a state where the paired PKR is most effective against a viral onslaught. “We showed that a small region of the HIV-1 genome termed TAR can regulate PKR,” Heinicke continued. “The caveat, however, is that this RNA must form a dimer in order to be an activator.” The extra length that dimer RNA provides is critical in encouraging PKR to pair up and function properly. “The length needed for one PKR to bind to RNA is 15 base pairs,” said Philip Bevilacqua, professor of chemistry, Penn State, one of the lead scientists on the project along with James Cole, associate professor, University of Connecticut. “to get two PKRs to bind and dimerize, you need an RNA strand that is twice as long.” Cole’s laboratory provided evidence of dimerization of RNA and PKR. In their experiments at Penn State, the scientists found the dimer RNA activated PKR from nine to 118 times more than the single strand RNA, depending on the RNA type. TAR RNA dimerization activated the most PKR when the TAR did not exhibit structural defects. The researchers report their findings in a recent issue of the Journal of Molecular Biology. “Adding these defects decreases the number of places where PKR can bind to the RNA,” Heinicke explained. RNAs that showed the greatest degree of symmetry are more potent PKR activators than ones with defects. “It appears as though length is a necessary but not sufficient condition for activation,” said Bevilacqua. The scientists constructed RNAs to remove TAR defects. Dimers of these RNAs increased PKR activity, compared to more asymmetric “wild-type” TAR dimers. Single strands of these RNAs did not activate PKR. this is in contrast to previous work, which reported that the single strand wild-type TAR showed a 50-fold increase of activation over more symmetric variants. “this helps us find what the actual molecular structure is that activates PKR,” said Bevilacqua. “It is still basic research for now, but finding the cause for this may ultimately lead to understanding disease.” Heinicke, Bevilacqua and Cole worked with Subba Rao Nallagatla, chemistry research associate, Penn State, University Park; Amy Diegelman-Parente, assistant professor of biochemistry, Penn State Altoona; Jason Wong, molecular and cell biology postdoctoral fellow, and Jeffrey Lary, analytical ultracentrifugation biotechnology facility scientist, University of Connecticut; and Xiaofeng Zheng, professor of biochemistry and molecular biology, University of Beijing. The NIH funded this project.

Published on: Mar 07 2012 09:10:53 PM EST  Updated on: Mar 08 2012 10:05:38 AM EST

South Florida doctor seeing cases of malaria

FORT LAUDERDALE, Fla. –

Dr. Ian Russinoff, an ER doctor with Broward General Medical Center has recently seen a few cases of malaria.

“I wouldn’t say we have a increased incidence of malaria but it needs to be something that’s kept on our radar because sometimes it’s a hard diagnosis to pinpoint and it’s potentially fatal,” Russinoff said.

Malaria is caused by a parasite that is passed from one person to another through the bite of an infected mosquito.

Malaria can also be transmitted from a mother to her unborn baby and through blood transfusions.

Symptoms include abdominal pain, headache, joint pain, nausea, sweating vomiting and fever.

The fever’s tend to come in cycles.  It’s going to come about every six hours,” said Russinoff.

A diagnosis is confirmed through blood work

“Once these parasites migrate to the liver you will get some break down of red blood cells which relates to the anemia we see in some of the lab findings,” Russinoff said.

Malaria is most common in tropical and subtropical areas and though not typical in the U.S., it has been introduced here from infected mosquitos that are transported into the country via airplanes.

Malaria will not resolve on it’s own and needs to be treated with antibiotics.

“It’s like any other infection if it runs its course and affects other parts of the body so it could be very serious,” said Russinoff.

Before traveling to warm climates outside the U.S., including the Caribbean, check with your doctor about taking an anti-malaria medication to prevent infection. d

• Copyright 2012 by Post Newsweek. All rights reserved. this material may not be published, broadcast, rewritten or redistributed.

Among the mechanisms of carcinogenesis are oncogene synthesis and expression, upregulation of cyclooxygenase, accelerated cell replication, failed apoptosis, viral activation, disruption of signaling pathways, autoimmunity, immunosuppression, angiogenesis and metastasis. All fall within the orbit of eicosanoids and the enzymes that synthesize them. Antidepressants may be of benefit in the prevention and treatment of cancer, as they inhibit the synthesis, antagonize the actions and accelerate the degradation of such eicosanoids as prostaglandins and thromboxanes.

Synthesized primarily by every cell membrane in the body, eicosanoids are ubiquitous in physiology and disease. Theessential fatty acid arachidonic acid (AA) is the primaryprecursor of such eicosanoids as prostaglandins(PGs), leukotrienes (LTs), thromboxanes (TXs) and lipoxins.

Since the identification of eicosanoids in1968 as potentially carcinogenic, an immense body of research has accumulated illuminating their ubiquitous role incancer. Isolation of isoforms of the PG-synthesizing enzymecyclooxygenase (COX) has stimulated interest in the potentialrole of selective COX-2 inhibitors in cancer treatment andprevention. the antiprostaglandin properties of antidepressants and their implications in cancer prevention and treatment have been neglected.

In 1968 Williams and coworkers reported high levels of PGs in the thyroid and plasma of patients with medullary cancer of thethyroid.[1] In 1976 Goodwin and coworkers reported increased synthesis of prostaglandin E2 (PGE2) in suppressor T-cells ofpatients with Hodgkin’s disease.[2] Numerous studies subsequently revealed elevated levels of PGsin solid tumors and in the immune cells and body fluids ofcancer patients.[3–12] Thousands of studies in animals and humans confirm the participation of eicosa- noids incarcinogenesis.[13–20]

PGs are involved in regulating the synthesis and expres- sion ofgenes and oncogenes. Genes and oncogenes in turn regulate suchPG-synthesizing enzymes as cyclo- oxygenase-2 (COX-2) andthe expression of PGs.[21–31]

The isolation of such isoforms of cyclooxygenase as COX-2 and the synthesis of selective COX-2 inhibitors havestimulated research into the expression of this isoform in cancer and its role in apoptosis. COX-2 overexpression converts procarcinogenstocarcinogens and inhibits apoptosis.

COX-2 is upregulated in such cancers as those of the head and neck, breast, lung, pancreas, bladder, cervix, prostate andmesothelium.32–45SuchPG-synthesis inhibitors as indomethacin andsulindac can induce regression of colon polyps in vivo andex vivo.[46] In population studies, chronic use of such PG-synthesis inhibitors as aspirin and ibuprofen has reduced the risk of colon cancer by as much as 50%.[47]

In 1983 Armato and Andreis reported that prostaglandinF1a and F2a intensely stimulate primary neonatal rat hepatocytes, F2a more powerfully stimulating DNA synth- esisthan arachidonic acid.[48]

In 1990 Goodlad and coworkersreported that the increase in gastric mucosal mass induced by misoprostol in the stomach of dogs is due to increased cell production. the increase in mucosal mass was the result of adramatic increase in the foveolar surface mucous cells.[49] Other studies have shown a para-doxical inhibitory effect of PGs on DNA synthesis.[50,51]

PGs and their synthesizing enzymes block apoptotic signals.such nonsteroidal anti-inflammatory compounds as sulindac andpiroxicam can induce apoptosis in normal and cancer cells.[52–57]Induction of PGs is essential if viruses, including the oncogenic, are to complete their replicative cycles.Indirectly, induction of PGs suppresses the antiviral activity of the immune system.[58,59]

Eicosanoids and their synthesizing enzymes are key factors in many signaling events. Disruptions of signaling pathways are incriminated in many cancers.[60–63]In a paradoxical counterpoint to immunosuppression, numerous autoimmune phenomena are reported in patients with cancer. Malignant tumors are diagnosed with increased frequency in patients with such auto-immune disorders as pemphigus, myasthenia gravis and the Eaton–Lambert syndrome. Apoptosis and PGs appear to play dual roles in autoimmunity and in cancer.[64–66]

Immunosuppression is both a cause and effect of cancer, avicious cycle.[67–70] Imai and his colleagues did an 11-year follow-up study to assess the level of naturalcytotoxic activity of such lymphocytes as natural killer (NK) cells and the incidence of cancer and death. their results showed that medium and high cytotoxic activity is associatedwith reduced cancer risk, and low activity is associated with increased cancer risk.[71]

Increase in PGs at the primary tumor focus may block surveillance by the immune system. PGs are potent suppressants of lymphocytes, and an increase in plasma PGs may contribute to a suppressive environment for lymphocyte function.

G.I. Deichman has shown that tumor progression in vivo isassociated with the appearance and selection of tumor cellswith a high level of antioxidant catabolizing activity and for the immediate release of prostaglandin E2 on contact with naturalkillers, macrophages and neu- trophils.

The expression of these phenotypes provides tumor cells with two mechanisms of local protection against effectors of innate and acquired antitumor activity. In primary viral carcinogenesis the selection of cells expressing these phenotypes begins within the latent period and can be completed by appearance of primary tumors.[72]

In 1983, Karmali and her coworkers reported that increased TX formation in human breast cancer specimensis associated with three clinical variables – tumor size, axillary lymph node metastases and distant metastases.the mechanisms in which PGs and TXs induce metastasis include induction of proteolyticenzyme production, neovascularization and subversion of the immune response.

The initiation of metastasis is thought to involve the adherence of circulating tumor cells to endothelial cells or to basement membranes. PGs and TXs play a role in adherence, with local TX concentrations possibly determining the sites of metastasis.[73–88]

The paraneoplastic syndrome includes a variety of neurological, hematological, metabolic cardiovascular and dermatological disorders. PGs are incriminated in many.[89–90]

Evidence from a variety of sources incriminates PGs in the pathogenesis of depression. Two-series PGs are elevated in the plasma,[91] spinal fluid,[92] and saliva of depressives,[93] and tranylcypromine directly lowers concentrations of the depressant prostaglandin D2 inthe brains of animals.[94] Infusion of prostacyclin, a two-series PG into patients withRaynaud’s disease as a vasodilator characteristically induces acutedepression.[95]

Horton’s 1966 report that PGs have powerful actions on thebrains of chicks and cats [96] stimulated intensive study of theactions of psychotropic drugs on PGs. Horrobin, Murphy and Wang and their coworkers showed that lithium carbonate inhibits prostaglandin E1 (PGE1).[97,98,99]

Recently, Chang showed that lithium decreases the turnover of arachidonate in various brain phospholipids.[100]

Lee showed that by inhibiting the mobilization of AA acid, antidepressants inhibit PGE2, with phenelzine (Nardil) exertinga more powerful antiprostaglandin effect than indomethacin.[101] Hong showed that tranylcypromine reduces the mobilization of archidonate,[102] while Horrobin and his coworkersshowed that such tricyclic antidepressants as imipramineand chlomipramine are weak PG agonists and powerful antagonists.[103]

Mtabaji and coworkers showed that tricyclicanti-depressants antagonize TXs.[104] Attempts to activate the primary prostaglandin degrading enzyme, 15-hydroxy- prostaglandindehydrogenase, failed until 1986, when Oi Mak and T.Chen showed that imipramine and amitriptyline have powerful activatory effects on this enzyme.[105]

Monoamine oxidase inhibitors, originally used in the treatmentof tuberculosis, have potent antiviral and immunoregulating properties. thus it is not surprising that one of them is effective in treating a neoplastic disease.

The disease is stage III and IV Hodgkin’s disease, the monoamine oxidase Matulane (procarbazine) part of the MOPP (nitrogen mustard, vincristine, procarbazine, prednisone) regimen.

In ignoring the actions ofmonoamine oxidase inhibitors on PGs, the manufacturer states, ‘There is evidence that the drug may act by inhibition of protein, RNA and DNA synthesis.’

In the Ward Jones lecture given at Manchester University in1957, Sir Heneage Ogilvie commented,

‘I have slowly come to frame in my mind an aphorism that can never be stated as such,because no statistics can be advanced to support it: ‘‘The happy man never gets cancer’’ the instances where the first recognizable onset of cancer has followed almost immediately on some disaster, bereavement, the breakup of a relationship, a financial crisis, or an accident are so numerous that they suggest that some controlling force that has hitherto kept the outbreakyincheck has been removed.[106]

In 1998 B. W. J. H. Penninx and her coworkers at the National Institute of Aging provided compelling support for Ogilvie’s hypothesis: chronically depressed people over theage of 70 are 88% more likely to develop cancer and twice as likely to die of it than their cheerful peers.[107]

In interstices between cell membrane phospholipids and genes,membrane phospholipids and organelles, genes and enzymes, genes and proteins, PGs induce cancer. the places where PG-synthesizing enzymes convert AA acidor phospholipids to PGs are possible sites of action ofantidepressants.

The ability of antidepressantsto alleviate or remit such autoimmune disorders as migraine, rheumatoid arthritis, asthma and multiple sclerosis strengthens the case for their potentialvalue in cancer.[108]

Depression incancer patients may be more an antecedent than a consequence of the disease.[121–124]

As depression lowers the threshold for stress and reduces compliance with adjuvant chemotherapy,[125] antidepres- sants may be of value inenhancing compliance. it would be surprising if the antiviral and immunostimulating properties alone of antidepressants did not lend themselves to cancer prevention and treatment.[112–120]

Other than the finding that lithium inhibits various phospholipases,[100] the actions of psychotropic agents on the arachidonic cascade has stimulated little recent research. the actions of antidepressants on such aspects of carcinogenesis as apoptosis, gene activation and suppression and the expression of COX and other enzymes appear to be fertile areas for basic and applied pharmacology.

The antiprostaglandin, antiviral and immunopotentiating properties of lithium carbonate suggest that it too is worthy of investigation in the prevention and treatment of cancer beyond that of its protective effects onhematopoeisis during chemotherapy.[126–134]

As the response to antidepressants is highly specific, many patients require multiple trials before their depression responds. Some subjects are refractory to all antidepressants and many relapse due to tachyphylaxis.[135]

PGs are capable of paradoxical pro-carcinogenic and anti-carcinogenic actions.[136-137].

Maintaining an index of suspicion, close clinical observation and limiting the duration of drug trials can mitigate such paradox.

1. Williams E. D., Karim S. M. M., Sandler M. Prostaglandin secretion bymedullary carcinoma of the thyroid. Lancet 1968;1: 22–23.

2. Goodwin J. S., Murphy S., Bankhurst A. D., et al. Prostaglandin-producing suppressor cells in Hodgkin’s disease. new Engl J Med1977; 297: 963–968.

3. Bennett A., Carter R. L., Stamford, I. F., Tanner N. S. B.Prostaglandin-like material extracted from squamous carcinomasof the head and neck. Br J Cancer 1980; 41:204–209.

4. Karmali R. A., Welt S., Thaler H. T., Lefevre F. Prostaglandins inbreast cancer: relationship to disease stage and hormone status. Br JCancer 1983; 48: 689–696.

5. Cooper C., Jones H. G., Weller R. O., Walker V. Production ofprostaglandins and thromboxane by isolated cells fromintracranial tumors. J Neurol Neurosurg Psych 1984; 47:579–584.

6. Amlot P. L., Chivers A., Heizelmann D., Youlten L. J. F. Increasedprostaglandin synthesis in Hodgkin’s disease: a lymphocyte-monocyte interaction. Adv Prost Thromb Res 1980; 6: 529–532.

7. Plescia O. J., Smith A. H., Grinwich K. Subversion of immune systemby tumor cells and role of prostaglandins. Proc Nat Acad Sci 1975;72(5): 1848–1851.

8. Balch C. M., Dougherty P. A., Tilden A. B. Excessiveprostaglandin E2 production by suppressor monocytes in head andneck cancer patients. Ann Surg 1982; 645–650.

9. Cameron D. J., Stromberg B. V. the ability of macrophages from headand neck cancer patients to kill tumor cells: effects of prostaglandininhibitors on cytotoxicity. Cancer 1984; 54(11):2403–2408.

10. Fiedler L., Zahradnik H. P., Schlegel G. Perioperative behavior ofprostaglandin E2 and 13,14 dihydro-15-keto-PGF2a in serum ofbronchial carcinoma patients. Adv Prost Thromb Res 1980;585–586.

11. Harvey P. R. C., Kimura L. H., Cripps C., Hokama Y. Distribution ofprostaglandins B, E and F series in plasma of cancer patients. J Med1981; 12(6): 427–432.

12. Bennett A., Berstock D. A., Harris M., Raja B., Rowe D. J. F.Prostaglandins and their relationship to malignant and benign breasttumors. Adv Prost Thromb Res 1980; 4: 595–600.

13. Karmali R. A., Sarkar N. H., Emerson W., good R. A.Prostaglandin regulation of murine mammary tumor virus production: abasis for some of the glucocorticoid and prolactin actions on mammarytumor cell cultures. Prosta Leuk Med1982; 9: 641–655.

14. Karmali R. A. Review: prostaglandins and cancer. ProstaglandinsMed 1980; 5: 11–28.

15. Bennett A., Houghton J., Leaper D. J., Stamford I. F. Cancergrowth, response to treatment and survival time in mice:beneficial effect of the prostaglandin synthesis inhibitorflurbiprofen. Prostaglandins 1979; 17(2): 179–191.

16. Popescu C. Z. the role of prostaglandins in the development ofmalignant melanoma in hamsters. Prosta Med 1981; 7: 321–325.

17. Cohen L. A., Karmali R. A. Endogenous prostaglandin production byestablished cultures of neoplastic rat mammary epithelial cells. In Vitro1984; 20(2): 119–126.

18. Lupulescu A. Enhancement of carcinogenesis by prostaglandins.Nature 1978; 272(13): 634–636.

19. Karmali R. A., Horrobin D. F., Ghayur T., Manku M. S., CunnaneT. C., et al. Influence of agents which modulatethromboxane A2 synthesis or action on R 3230AC mammarycarcinoma. Cancer Letters 1978; 5: 205–208. Prostaglandins, Leukotrienes and Essential Fatty Acids (2001) 65(5&6), 233^239

20. Quia L., Kozoni V., Tsioulias G. J., Koutsos M. I., Hanif R. Selectedeicosanoids increase the proliferation of human colon carcinoma cell linesand mouse monocytes in vivo. Biochem Biophys Acta 1995; 1258(2):215–223.

21. Hermann C., Block C., Geisen C., Haas K., Weber C., et al.Sulindac sulfide inhibits Ras signaling. Oncogene 1998; 17(14):1769–1776.

22. Ramsay R. G., Friend A., Vizantios Y., Freeman R., Sicurella C., et al.Cyclooxygenase-2, a colorectal cancer nonsteroidal anti- inflammatorydrug target, is regulated by c-MYB. Cancer Res2000; 60(7): 1805–1809.

23. Fitzgerald J., Edietz T. J., Hughes-Fulford M. ProstaglandinE2-induced up-regulation of c-fos messenger ribonucleic acidis primarily mediated by 3’,5’-cyclic adenosine monophosphate inMC3T3-E1 osteoblasts. Endocrinology 2000; 141(1):291–298.

24. Honn K. V., Dunn J. R., Morgan L. R., Bienkowski M., Marnett L. J.Inhibition of DNA synthesis in Harding–Passey melanoma cells byprostaglandins A1 and A2: comparison with chemotherapeutic agents.Biochem Biophys Res Comm 1979;87(3): 795–801.

25. Hughes-Wiley M. H., Feingold K. R., Grunfeld C., Quesney- Huneeus V.,Wu J. M. Evidence for c-AMP independent inhibition of S-phase DNAby prostaglandins. J Biol Chem 1983;258(1): 491–496.

26. Hughes-Fulford M., Wu J., Kato T., et al. Inhibition of DNA synthesisand cell cycle by prostaglandins independent of cyclic AMP. AdvProstaglandin Thromboxane Leukot Res 1985; 15:401–404.

27. Hughes-Fulford M. Prostaglandin regulation of gene expression andgrowth in normal and malignant tissues. Adv Exp Med Biol1997; 400A: 269–278.

28. Sinha D., Addya S., Murer E., Boden G. 15-Deoxy-delta (12,14)prostaglandin J2: a putative endogenous promoter of adipogenesissuppresses the ob gene. Metabolism 1999; 48(6):786–791.

29. Choudry M. A., Uddin S., Sayeed M. M. Prostaglandin E2modulation of p59fyntyrosine kinase in T-lymphocytes during sepsis. JImmunol 1998; 160(2): 929–935.

30. Kim J. S., Chae H. D., Joh T. H., et al. Stimulation of human DBHgene expression by prostaglandin E2 in human neuroblastomaSK-N-BE(2)C cells. J Mol Neurosci 1997; 9: 143–150.

31. Pinelli E., Poux N., Garren L., et al., Activation of mitogen- activatedprotein kinase by fumonisin B(1) stimulates cPLA(2) phosphorylation,the arachidonic acid cascade and CAMPproduction. Carcinogenesis 1999; 20: 1683–1688.

32. Sheng H., Williams C. S., Shao J., Liang P., Dubois R. N.,Beauchamp R. D. Induction of cyclooxygenase-2 by activatedHa-ras oncogene in Rat-1 fibroblasts and the role of mutated proteinkinase pathway. J Biol Chem 1998; 273(34):22121–22427.

33. Emond V., Fortier M. A., Murphy B. D., Lambert R. D.Prostaglandin E2 regulates both interleukin-2 and granulocyte-macrophage colony-stimulating factor gene expression in bovinelymphocytes. Biol Reprod 1998; 568(1): 143–151.

34. Gilhooly E. M., Rose D. P. the association between a mutated rasgene and cyclooxygenase-2 expression in human breast cancer cell lines.Int J Oncol 1999; 15(2): 267–270.

35. William C. S., Mann M., Dubois R. N. the role ofcyclooxygenases in inflammation, cancer and development.Oncogene 1999; 18(55): 7908–7916.

36. Fosslien E. Molecular pathology of cyclooxygenase-2 inneoplasia. Ann Clin Lab Sci 2000; 30(1): 3–21. Review: antidepressants, eicosanoids and cancer 237

37. Chan G., Boyle J. O., Yang E. K., Zhang F., Sacks P. G., et al.Cyclooxygenase-2 expression is upregulated in squamous cellcarcinoma of the head and neck. Cancer Res 1999; 59(5):991–994.

38. Achiwa H., Yatabe Y., Hida T., Kuroishi T., Kozaki K., et al.Prognostic significance of elevated cyclooxygenase 2 expressionin primary, resected lung adenocarcinomas. Clin Cancer Res 1999;5(5): 1001–1005.

39. Watkins D. N., Lenzo J. C., Segal A., Garlepp M. J., Thompson P. J.Expression and localization of cyclooxygenase isoforms in non- smallcell lung cancer. Eur Resp J 1999; 14(2): 412–418.

40. Molina M. A., Sitja-Arnau M., Lemoine M. G., Frazier M. L.,Sinicrope F. A. Increased cyclooxygenase-2 expression in humanpancreatic carcinomas and cell lines: growth inhibition by nonsteroidalanti-inflammatory drugs. Cancer Res 1999;59(17): 4356–4362.

41. Sawaoka H., Kawano S., Tsuji S., Tsugi M., Sun W., et al.Helicobacter pylori infection induces cyclooxygenase-2 expressionin human gastric mucosa. Prostaglandins Leukot Essent Fatty Acids1998; 59(5): 313–316.

42. Murata H., Kawano S., Tsuji S., Tsuji M., Sawaoka H., et al.Cyclooxygenase-2 overexpression enhances lymphatic invasion andmetastasis in human gastric carcinoma. Am J Gastroenterol1999; 94(2): 451–455.

43. Yoshimura R., Sano H., Masuda C., Kawamura M., Tsubouchi Y.Expression of cyclooxygenase-2 in prostatic carcinoma. Cancer2000; 89(3): 589–596.

44. Marrogi A., Pass H. I., Khan M., Metheny-Barlow I. J., Harris C.C., Gerwin B. I. Human mesothelioma samples overexpress bothcyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (NOS2):in vitro antiproliferative effects of a COX-2 inhibitor.Cancer Res 2000; 60(14): 3696–3700.

45. Taketo M. M. Cyclooxygenase-2 inhibitors in tumorigenesis(part 1). J Natl Cancer Inst 1998; 90(20): 1529–1536.

46. Al-Saleem T. Skin cancers in xeroderma pigmentosum: response toindomethacin and steroids. Lancet 1980; 264–266.

47. Thun M. J., Namboordiri M. M., Heath C. W. Jr. Aspirin use andreduced risk of fatal colon cancer. N Engl J Med 1991; 325:1593–1956.

48. Armato U., Andreis P. G. Prostaglandins of the F series areextremely powerful growth factors for primary neonatal rathepatocytes. Life Sci 1983; 33: 1745–1755.

49. Goodlad R. A., Madgwick A. J., Moffatt M. R., et al. Prostaglandinsand the dog stomach: effects of misoprostol on the proportion ofmucosa to muscle and on the proportion of different epithelial typecells. Digestion 1990; 45: 212–216.

50. Nilsson J., Olsson A. G. Prostaglandin E1 inhibits DNA synthesisin arterial smooth muscle cells stimulated with platelet-derived growthfactor. Atherosclerosis 1984; 53: 77–82.

51. Smith D. L., Willis A. L., Mahmud I. Eicosanoid effects on cellproliferation in vitro: relevance to atherosclerosis. Prosta LeukMed 1984; 16: 1–10.

52. Waddell W. R. Stimulation of apoptosis by sulindac andpiroxicam. Clin Sci (Colch) 1998; 95(3): 385–388.

53. Lim J. T., Piazza G. A., Han E. K., et al. Sulindac derivatives inhibitgrowth and induce apoptosis in human prostate cancer cell lines.Biochem Pharmacol 1999; 58: 1097–1107.

54. Kusuhara H., Matsuyuki H., Matsuura M., Imayoshi T.,Okumoto T., et al. Induction of apoptotic DNA fragmentation bynonsteoidal anti-inflammatory drugs in cultured rat gastric mucosalcells. Eur J Pharmacol 1998; 360(2–3): 273–280.

55. Dittmann K. H., Mayer C., Rodemann H. P., et al. MK-886, aleukotriene biosynthesis inhibitor induces antiproliferative effects andapoptosis in HL-60 cells. Leuk Res 1998; 22: 49–53.

56. Kawamura T., Horie S., Maruyama T., Akira T., Imagawa T.,Prostaglandin E1 transported into cells blocks the apoptotic signalsinduced by nerve growth factor deprivation. JNeurochem 1999; 72(5): 1907–1914.

57. Baliff B. A., Mincek N. V., Barratt J. T., et al. Interactionof cyclooxygenases with an apoptosis- and autoimmunity-associated protein. Proc Natl Acad Sci USA 1996; 93:5544–5549.

58. Dore-Duffy P. Differential effect of prostaglandins and otherproducts of arachidonic acid metabolism on measles virusreplication in vero cells. Prosta Leuk Med 1982; 8:73–82.

59. Wahl L. M., Corcoran M. L., Pyle S. W., et al. Human immunodeficiencyvirus glycoprotein (gp 120) induction of monocyte arachidonic acid andinterleukin 1. Proc Natl Acad Sci USA 1989; 86: 621–625.

60. Schaad N. C., Magistretti P. J., Schorderet M. Prostanoids andtheir role in cell-cell interactions in the central nervous system.Neurochem Int 1991; 18(3): 303–322.

61. Villaneuva A., Garcia C., Paules A. B., Vicente M., Megias M.Disruption of the antiproliferative TGF-b signaling pathways in humanpancreatic cancer cells. Oncogene 1998; 17(15):1969–1978.

62. Di Battista J. A., Martel-Pelletier J., Pelletier J. Suppression of tumornecrosis factor (TNFa) gene expression by prostaglandin E2. Role of earlygrowth response protein-1 (Egr-1). Osteoarthritis Cartilage 1999; 7(4):395–398.

63. Moreno J. J. Regulation of arachidonic acid release and prostaglandinformation cell-to-cell adhesive interactions in wound repair. PflugersArch 1997; 433: 351–356.

64. Houssiau F. A., Kirkove C., Asherson R. A., Hughes G. R. V.,Timothy A. R. Malignant lymphoma in systemic rheumatic diseases. A report of five cases. Clin Exp Rheum 1991; 9:515–518.

65. Sela O., Shoenfeld Y. Cancer and autoimmune diseases. SeminArthritis Rheum 1988; 18: 77–87.

66. Isomaki H. A., Hakulinen T., Joutsenlahti U. Excess risk oflymphomas, leukemia and myeloma in patientswith rheumatoid arthritis. J Chronic Dis 1978; 31:691–696.

67. Young M. R., Dizer M. Enhancement of immune function and tumorgrowth inhibition by antibodies against prostaglandin E2. Immunol Comm1983; 12(1): 11–23.

68. Leung K. H., Mihich E. Prostaglandin modulation of development ofcell-mediated immunity in culture. Nature1980; 288: 597–600.

69. Dilman V. R. Metabolic immunosuppression which increases the riskof cancer. Lancet 1977; ii: 1207–1210.

70. Buda J. A., Suciu-Foca N., Blomain E., McManus S., Reemtsma K.Impaired cell-mediated immunity in patients with cancer. J SurgOnc 1975; 7: 525–529.

71. Imai K., Matsuyama S., Miyake S., Suga K., Nakachi K. Naturalcytotoxic activity of peripheral-blood lymphocytes and cancer incidence:an 11-year follow up study of a general population. Lancet 2000; 356:1795–1799.

72. Deichman G. I. Natural selection and early changes ofphenotype of tumor cells in vivo: acquisition of new defensemechanisms. Biochemistry (Mosc) 2000; 65(1): 78–94.

73. Peterson H. I. Tumor angiogenesis inhibition by prosta-glandin synthase inhibitors. Anticancer Research 1986; 6:251–254.

74. Chiarugi V., Magnelli L., Gallo O. COX-2, iNOS and p53 as playmakersof tumor angiogenesis (review). Int J Mol Med 1998;2(6): 714–720. Prostaglandins, Leukotrienes and Essential Fatty Acids (2001) 75. Damtew B., Spagnuolo P. J. Tumor cell-endothelial cell interactions:evidence for roles for lipoxygenase products of arachidonic acid inmetastasis. Prostaglandins Leukot Essential Fatty Acids 1978; 56(4):295–300.

76. Fulton A. M. Inhibition of experimental metastasis withindomethacin: role of macrophages and natural killer cells.Prostaglandins 1988; 35(3): 13–42.

77. Tisdale M. J. Role of prostaglandins in metastatic dissemination ofcancer: minireview on cancer research. Expl Cell Biol 1983;51: 250–256.

78. Daniel T. O., Liu H., Morrow J. D., Crews B. C., Marnett L. J.Thromboxane A2 is a mediator of cyclooxygenase dependentendothelial migration and angiogenesis. Cancer Res 1999;59(18): 4574–4577.

79. Fulton A. M. Interactions of natural effector cells andprostaglandins in the control of metastasis. JNCI 1987; 78:735–740.

80. Stringfellow D., Fitzpatrick F. Prostaglandin D2 controls pulmonarymetastasis of malignant melanoma cells. Nature1979; 282: 76–78.

81. Nanji A. A. Thromboxane synthase and organ preference formetastases. new Eng J Med 1979; 138–139.

82. Fantone J. C., Elgas L. J., Weinberger L., Varani J. Modulation of tumorcell adherence by prostaglandins. Oncology 1983; 40:421–426.

83. Honn K. V., Cicone B., Skoff A. Prostacyclin: a potentantimetastatic agent. Science 1981; 212: 1270–1272.

84. Duffy C. P., Elliott C., O’Connor R. A., Heenan M. M., Coyle S., etal. Enhancement of chemotherapeutic drug toxicity to human tumorcells in vitro by a subset of non-steroidal anti- inflammatory drugs(NSAIDs). Eur J Cancer 1998; 34(8):1250–1259.

85. Greaves K., Ibbotson K. J., Atkins D., Martin T. J. Prostaglandins asmediators of bone resorption in renal and breast tumors. Clin Sci 1980;58: 201–210.

86. Kaneti J., Thomson M. P., Reid C. R. Prostaglandin E2 affects thetumor immune response in prostatic cancer. J Urol 1981; 126:65–70.

87. Lala P. K., Elkashab M., Kerbel R. S. W., Parhar R. S. Cure of humanmelanoma lung metastases in nude mice with chronic indomethacintherapy combined with multiple rounds of IL-2: characteristics of killercells generated in situ. Int Immunol1990; 2(12): 1149–1158.

88. Rosenberg L., Palmer J. R., Zauber A. G., Warshauer M. E., Stolley P.D., et al. A hypothesis: non-steroidal anti-inflammatory drugs reduce theincidence of large-bowel cancer. J Natl Cancer Inst1991; 83: 355–358.

89. Minna J. D., Bunn P. A. Jr. Paraneoplastic syndromes.In: Devita V. T. et al., eds. Philadelphia: Lippincott, Principles andPractices of Oncology. 1982; 1476–1517.

90. Grunwald G. B., Simmonds M. A., Klein R., Kornguth S. E.Autoimmune basis for visual paraneoplastic syndrome in patientswith small-cell lung carcinoma. Lancet 1985; 1:658–661.

91. Lieb J., Karmali R., Horrobin D. Elevated levels of prostaglandinE2 and thromboxane B2 in depression. Prostaglandins LeukotMed 1983; 10: 361–367.

92. Linnoila M., Whorton A. R., Rubinow D. K. CSF prostaglandin levelsin depressed and schizophrenic patients. Arch Gen Psychiatry 1983;40: 405–406.

93. Ohishi K., Ueno R., Nishino S. Increased level of salivaryprostaglandins in patients with major depression. Biol Psychiatry1988; 23: 326–334. Prostaglandins, Leukotrienes and Essential Fatty Acids (2001) 65(5&6), 233^239

94. Ellis E. F., Rosenblum W. I., Birkle D. L. Lowering of brain levels ofthe depressant prostaglandin D2 by the antidepressant tranylcypromine.Biochem Pharmacol 1982; 31: 1783–1784.

95. Ansell D., Belch J. J., Forbes C. D. Depression and prostacyclininfusion. Lancet 1986; 2: 1203–1205.

96. Horton E. W. Actions of prostaglandins E1, E2 and E3 on the centralnervous system. Brit J Pharmacol 1964: 22: 189–192.

97. Horrobin D. F., Mtabaji J. P., Manku M. S., et al. Lithium as a regulatorof hormone-stimulated prostaglandin synthesis. In:Johnson F. N., Johnson F. Lithium in Medical Practice. Baltimore, MD:University Park Press, 1978; 243–263.

98. Murphy D. L., Donnelly C., Moskowitz J. Inhibition by lithium ofprostaglandin E1 and norepinephrine effects on cyclicadenosine monophosphate production in human platelets. ClinPharm Therap 1973; 15(5): 810–815.

99. Wang Y-C., Pandey G. M., Mendels J., Frazier A. Effect of lithium onprostaglandin E1 stimulated adenyl cyclase activity of human platelets.Biochem Pharmacol 1974; 23: 845–855.

100. Chang M. C. J., Grange E., Rabin O., et al. Lithium decreasesturnover of arachidonate in several brain phospholipids.Neurosci Lett 1996; 230: 171–174.101. Lee R. E. the influence of psychotropic drugs on prostaglandinbiosynthesis. Prostaglandins 1974; 51: 63–68.

102. Hong S. H., Carty T., Deykin D. Tranylcypromine and 15-hydroperoxyarachidonate effect arachidonic acid release in additionto inhibition of prostacyclin synthesis in calf aortic endothelial cells. JBiol Chem 1980; 2455(20): 9538–9540.

103. Manku M. S., Horrobin D. F. Chloroquine, quinine, procaine,quinidine and clomipramine are prostaglandin agonists andantagonists. Prostaglandins 1976; 12: 789–801.

104. Mtabaji J. P., Manku M. S., Horrobin D. F. Actions of the tricyclicantidepressant clomipramine on responses to pressor agents:interactions with prostaglandin E2. Prostaglandins 1977; 14:125–132.

105. Mak O., Chen S. Effects of two antidepressant drugs-imipramine andamitriptyline on the enzyme activity of 15-hydroxyprostaglandin dehydrogenase purified from brain, lung, liverand kidney of mouse. Prog Lipid Res 1986; 25: 153–155.

106. Ogilvie H. the Human Heritage (the Ward Jones lecture,Manchester University). Lancet, July 6th, 1957.

107. Penninx B. W., Guralnik J. M., Pahor M., Ferruci L., Cerhan J. R. et al.Chronically depressed mood and cancer risk in older persons. J NatlCancer Inst 1998; 90(24): 1888–1893.

108. Lieb J. Remission of rheumatoid arthritis and other disorders ofimmunity in patients taking monoamine oxidase inhibitors. Int JImmunopharmacol 1983; 5: 353–357.

109. Magni G., Conlon P., Arsie D. Tricyclic antidepressants in thetreatment of cancer pain: a review. Pharmacopsychiat 1987; 20:160–164.

110. Botney M., Fields H. L. Amitriptyline potentiates morphine analgesiaby direct action on the central nervous system. Ann Neurol 1983;13(2): 160–164.

111. Breitbart W. Psychotropic adjuvant analgesics for pain in cancerand AIDS. Psychooncology 1998; 7(4): 333–345.

112. Lieb J. Invisible antivirals. Int J Immunopharmacol 1994; 16: 1–5.

113. Rosenthal S. H. Does phenelzine relieve aphthous ulcers of the mouth?new Engl J Med 1984; 311: 1442.

114. Rosenthal S. H., Fitch W. P. the antiherpetic effect of phenelzine.J Clin Psychopharmacol 1987; 7: 119.

115. Lofft J. MAO inhibitors. Psychiat Times 1985; 11.

116. Ali B. H., Bartlet A. L. Inhibition of monoamine oxidase inchickens and ducklings by a microbial metabolite of furazolidone.Q J Exp Physiol 1982; 67: 69–79. Review: antidepressants, eicosanoids and cancer 239 117. Zilberstein D., Dwyer D. M. Antidepressants cause lethaldisruption of membrane function in the human protozoan parasiteLeishmania. Science 1984;118.Weinbach E. C., Costa J. L., Wieder S. C. Antidepressant drugssuppress growth of the human pathogenic protozoan Giardia lamblia.Res Commun Chem Pathol Pharmacol 1985; 47:145–148.

119. Bitonti A. J., Sjoerdsma A., McCann P. P., et al. Reversal ofchloroquine resistance in malaria parasite Plasmodiumfalciparum by desipramine. Science 1988; 242: 1301–1303.

120. Salama A., Facer C. A. Desipramine reversal of chloroquineresistance in wild isolates of Plasmodium falciparum. Lancet1990; 335: 164–165.

121. Fulton C. the prevalence and detection of psychiatric morbidity inpatients with metastatic breast cancer. Eur J Cancer Care(Engl) 1998; 7(4): 232–239.122. Bottomley A. Depression in cancer patients: a literature review.Eur J Cancer Care (Engl)1998; 7(3): 181–191.

123. Pirl W. F., Roth A. J. Diagnosis and treatment of depression in cancerpatients. Oncology (Huntingt) 1999; 13(9): 1293–1301.

124. Kugaya A., Akechi T., Nakano T., Okamura H., Shima Y., et al.Successful antidepressant treatment for five terminally ill cancerpatients with major depression Suicidal ideation and a desire for death.Support Care Cancer 1999; 7(6): 432–436.

125. Colleoni M., Mandala M., Perruzotti G., Robertson C., Bredart A., et al.Depression and degree of acceptance of adjuvant cytotoxic drugs. Lancet2000; 356: 1326–1327.

126. Lieb J. Remission of recurrent herpes during therapy with lithium.N Eng J Med 1979; 301: 942.

127. Amsterdam J. D., Maislin G., Rybakowski J. A possible antiviral actionof lithium carbonate in herpes simplex virus infections. Biol Psychiatry1990; 27: 447–453.

128. Lieb J. Remission of herpes virus infection and immunopotentiationwith lithium carbonate: inhibition of prostaglandin E1 may explain its antiviral, immunopotentiating andantimanic properties. Biol Psychiatry 1981; 695–698.

129. Lieb J. Lithium and immune function. Med Hypotheses 1987; 23:73–93.Skinner G. R., Hartley C., Buchan A., et al. the effect of lithium chlorideon the replication of herpes simplex virus. Med Microbiol Immunol1980; 168: 139–148.

130. Hansell N. Manic illness presenting with physical symptoms.Am J Psychiatry 1996; 147: 11.Cohen Y., Chetrit A., Cohen Y., Sirota P., Modam B. Cancermorbidity in psychiatric patients: influence of lithium carbonatetreatment. Med Oncol 1998; 15(1): 32–36.

131. Ravischandran D., Cooper A., Johnson C. D. Effect of lithiumgamma-linolenate on the growth of experimental human pancreaticcarcinoma. Br J Surg 85(9): 1201–1205.

132. Steinherz P. G., Rosen G., Giavini F., Wang Y., Miller D. R. the effectof lithium carbonate on leukopenia after chemotherapy. J Ped PharmTher 1980; 96(5): 923–927.

133. Lieb J., Balter A. Antidepressant tachyphylaxis. Med Hypoth1984; 15: 279–291.

134. Fukushima M., Kato M. Antitumor marine icosanoids:clavulones and punaglandins. Adv Prost Thromb and Leuk Res1985; 15: 415–418.

135. Fukushima M., Kato M. Antineoplastic prostaglandin: antitumor effect of PGA and PGJ derivatives. In: Thaler-Dao H., et al. eds. Icosanoids andcancer. new York: Raven Press, 275–278.

136. Cotterchio M., Kreiger N., Darlington G., Steingart A.Antidepressant medication use and breast cancer risk. Am JEpidemiol 2000; 151(10): 951–957.

137. Damluji N. F., Ferguson J. M. Paradoxical worsening ofdepressive symptomatology caused by antidepressants. J ClinPsychopharm 1988; 8(5): 347–349.

The cause of a mysterious condition that haunts its sufferers with sensations of crawling bugs and fibrous material embedded in the skin may be one step closer to being found, a new study suggests.

The condition, commonly referred to as Morgellons, does not appear to be contagious, according to a new report from the Centers for Disease Control and Prevention.

“This alleviates concerns about the condition being contagious between family members and others,” said mark Eberhard, Director of CDC’s Division of Parasitic Diseases and Malaria.

People with Morgellons report having symptoms manifesting on their skin. These include non-healing skin lesions, the emergence of fibers or solid material from the skin, and disturbing sensations, such as crawling, stinging or biting. Some patients report fatigue, memory loss and a substantial decline in quality of life, according to the study.

The study was undertaken after the CDC received a number of calls over the last 10 years with reports of the condition, Eberhard said.

“We had no idea what it was or might be,” Eberhard told MyHealthNewsDaily. “We felt very compelled to do something. it was quite clear that people were suffering.”

The report still does not identify a cause of the condition, and Morgellons is not recognized as a distinct medical disorder. however, by ruling out an infectious cause, researchers have begun to narrow down what health care providers need to look for when patients report signs of the condition, Eberhard said. And it’s likely that different factors contribute to individual cases.

“I don’t think there’s going to be a single diagnosis that will fit across the spectrum of it,” Eberhard said.

Unexplained disease

Eberhard and colleagues identified 109 patients with this condition by searching the electronic medical record database of Kaiser Permanente of Northern California. The researchers estimate the condition is rare, found in about four out of every 100,000 people.

Patients were put through a battery of tests to identify possible causes, including a medical exam, skin biopsies and psychiatric and blood testing. Fibers and solid material was extracted from the patients’ wounds, and their composition was examined.

“There’s been a great deal of fixation, on everybody’s part, with those fibers,” Eberhard said. Previous reports included patients bringing fibers they said had emerged from their skin to their doctors, but “there was no way to validate, scientifically, where the fibers came from,” Eberhard said.

The researchers concluded the fibers were coming from external sources, mostly from cotton. Fibers from clothing or carpet may become stuck in an open wound before it clots over, and appear to be coming from the wound, Eberhard said.

The majority of patients were middle-age white women. about half had evidence of other medical conditions, mostly psychiatric illnesses. Also, about half of patients were found to have been using drugs, including amphetamines, opiates and cocaine, according to the study.

Most of the lesions had the appearance of wounds caused by scratching, Eberhard said. Other potential causes for some of the cases include eczema and bug bites.

Seeking help

Eberhard emphasized that the study cannot say whether certain factors, including drug use and scratching, are a cause or an effect of the condition.

People who suspect they have Morgellons should speak with their health care provider, Eberhard said. Eberhard recommends that both the patient and doctor keep an open mind about the diagnosis.

However, “we would propose that they not focus on an infectious cause, or an environmental link,” Eberhard said.

Although no treatment for Morgellons is available, patients should be given standard therapies for any co-occurring conditions they may have, the researchers say. in addition, patients may benefit from therapies used to treat psychiatric conditions with similar symptoms.

The study is published today (Jan. 25) in the online journal PLoS ONE.

• Hypersex to Hoarding: 7 New Psychological Disorders
• 9 weirdest Allergies
• 7 weirdest Medical Conditions

Pocketless trousers as a strategy to fight corruption in Nepal (h/t Judah Grunstein).

Lay off trashing the moon landings, okay? It was cool to walk on the moon.

Caterpillars taking over West Africa are nothing; the latest insectine invasion is of Argentine super ants, who’ve got their eyes (?) set on colonizing the entire world.

And…don’t forget the food crisis in Africa.