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There are different classes of antiretroviral drugs that act at different stages of the HIV life-cycle.

Antiretroviral (ARV) drugs are broadly classified by the phase of the retrovirus life-cycle that the drug inhibits.

• Nucleoside and nucleotide reverse transcriptase inhibitors (NRTI) inhibit reverse transcription by being incorporated into the newly synthesized viral DNA strand as a faulty nucleotide. This causes a chemical reaction resulting in DNA chain termination.
• Non-nucleoside reverse transcriptase inhibitors (NNRTI) inhibit reverse transcriptase directly by binding to the enzyme and interfering with its function.
• Protease inhibitors (PIs) target viral assembly by inhibiting the activity of protease, an enzyme used by HIV to cleave nascent proteins for final assembly of new virons.
• Integrase inhibitors inhibit the enzyme integrase, which is responsible for integration of viral DNA into the DNA of the infected cell. There are several integrase inhibitors currently under clinical trial, and raltegravirbecame the first to receive FDA approval in October 2007.
• Entry inhibitors (or fusion inhibitors) interfere with binding, fusion and entry of HIV-1 to the host cell by blocking one of several targets. Maraviroc and enfuvirtide are the two currently available agents in this class.
• CCR5 receptor antagonists are the first antiretroviral drugs which do not target the virus directly. Instead, they bind to the CCR5 receptor on the surface of the T-Cell and block viral attachment to the cell. Most strains of HIV attach to T-Cells using the CCR5 receptor. If HIV cannot attach to the cell, it cannot gain entry to replicate.
• Maturation inhibitors inhibit the last step in gag processing in which the viral capsid polyprotein is cleaved, thereby blocking the conversion of the polyprotein into the mature capsid protein (p24). Because these viral particles have a defective core, the virions released consist mainly of non-infectious particles. Alpha interferon is a currently available agent in this class.Two additional ones under investigation arebevirimat and Vivecon.

Combination therapy

The life cycle of HIV can be as short as about 1.5 days from viral entry into a cell, through replication, assembly, and release of additional viruses, to infection of other cells. HIV lacks proofreading enzymes to correct errors made when it converts its RNA into DNA via reverse transcription. Its short life-cycle and high error rate cause the virus to mutate very rapidly, resulting in a high genetic variability of HIV. Most of themutations either are inferior to the parent virus (often lacking the ability to reproduce at all) or convey no advantage, but some of them have a natural selection superiority to their parent and can enable them to slip past defenses such as the human immune system and antiretroviral drugs. The more active copies of the virus the greater the possibility that one resistant to antiretroviral drugs will be made.

When antiretroviral drugs are used improperly, these multi-drug resistant strains can become the dominant genotypes very rapidly. Improper serial use of the reverse transcriptase inhibitors zidovudine, didanosine,zalcitabine, stavudine, and lamivudine can lead to the development of multi-drug resistant mutations. The mutations can include the V75I, F77L, K103N, F116Y, Q151M, and the M184V mutation. These mutations were observed before protease inhibitors had come into widespread use. The mutants retained sensitivity to the early protease inhibitor saquinavir. These mutants were also sensitive to the rarely used reverse transcriptase inhibitor foscarnet.

Antiretroviral combination therapy defends against resistance by suppressing HIV replication as much as possible.

Combinations of antiretrovirals create multiple obstacles to HIV replication to keep the number of offspring low and reduce the possibility of a superior mutation. If a mutation that conveys resistance to one of the drugs being taken arises, the other drugs continue to suppress reproduction of that mutation. With rare exceptions, no individual antiretroviral drug has been demonstrated to suppress an HIV infection for long; these agents must be taken in combinations in order to have a lasting effect. As a result, the standard of care is to use combinations of antiretroviral drugs. Combinations usually comprise two nucleoside-analogue RTIs and one non-nucleoside-analogue RTI or protease inhibitor.This three drug combination is commonly known as a triple cocktail.

Combinations of antiretrovirals are subject to positive and negativesynergies, which limits the number of useful combinations.

In recent years, drug companies have worked together to combine these complex regimens into simpler formulas, termed fixed-dose combinations. For instance, two pills containing two or three medications each can be taken twice daily.This greatly increases the ease with which they can be taken, which in turn increases adherence, and thus their effectiveness over the long-term. Lack of adherence is a cause of resistance development in medication-experienced patients. Patients who maintain proper therapy can stay on one regimen without developing resistance. This greatly increases life expectancy and leaves more drugs available to the individual should the need arise.

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The Ebola virus first came to notice in 1976 in outbreaks of Ebola hemorrhagic fever in Zaire and Sudan. The strain of Ebola which broke out in Zaire has one of the highest case fatality rates of any human pathogenic virus, roughly 90%. The strain which broke out later in Sudan has a mortality of approximately 50%. The virus is believed to be initially transmitted to a human via contact with an infected animal host. From the first human infected, the virus is then transmitted by human contact with infected blood and bodily fluids of a diseased person, and by human contact with contaminated medical equipment, such as needles. Both of these infectious mechanisms will occur in clinical (nosocomial) and non-clinical situations. Due to the high fatality rate, the rapidity of demise, and the often remote areas where infections occur, the potential for widespread epidemic outbreaks is considered low.

Ebola is believed to be a zoonotic virus as it is currently devastating the populations of lowland gorillas in Central Africa. As of late 2005, three species of fruit bat were identified as carrying the virus, and did not exhibit symptoms, and are now believed to be the natural host species, or reservoir, of the virus.

Ebola hemorrhagic fever is potentially lethal and encompasses a range of symptoms including fever, vomiting, diarrhea, generalized pain or malaise, and sometimes internal and external bleeding. Mortality rates are extremely high, with the human case-fatality rate ranging from 50% – 89%, according to viral subtype. The cause of death is usually due to hypovolemic shock or organ failure.

Because Ebola is potentially lethal and since no approved vaccine or treatment is available, Ebola is classified as a biosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare and was investigated for that use by both the Soviet Union and the United States during the Cold War. Its effectiveness as a biological-warfare agent is compromised by its extreme deadliness and its level of contagion: a typical outbreak spreads through a small village or hospital, affects the entire population, and then runs out of potential hosts, burning out before it reaches a larger community. Also important is that none of the strains of Ebola known to cause disease in humans have been found to be airborne; only the strain known as Ebola Reston (after the city of Reston, Virginia where it was first identified in Green Monkeys) is believed to be airborne.

Microbiologists have defined several subtypes of Ebola. The following list is not exclusive. A new strain of Ebola has been identified in Uganda during an outbreak. It does not match any of the four Ebola subtypes previously identified by scientists.

Zaïre ebola virus
Known human cases and deaths during outbreaks of Zaïre Ebolavirus between 1976 and 2003
Known human cases and deaths during outbreaks of Zaïre Ebolavirus between 1976 and 2003

The Zaïre Ebola virus has the highest mortality rate, up to 90% in some epidemics, with an average of approximately 83% mortality over 27 years. The case-fatality rates were 88% in 1976, 100% in 1977, 59% in 1994, 81% in 1995, 73% in 1996, 80% in 2001-2002 and 90% in 2003. There have been more outbreaks of Zaïre Ebola virus than any other strain.

The first outbreak took place on August 26, 1976 in Yambuku, a town in the north of Zaïre. The first recorded case was Mabalo Lokela, a 44-year-old schoolteacher returning from a trip around the north of the state. His high fever was diagnosed as possible malaria and he was subsequently given a quinine shot. Lokela returned to the hospital every day. A week later, his symptoms included uncontrolled vomiting, bloody diarrhea, headache, dizziness, and trouble breathing. Later, he began bleeding from his nose, mouth, and anus. Lokela died on September 8, 1976, roughly 14 days after the onset of symptoms.

Soon after, more patients arrived with varying but similar symptoms including fever, headache, muscle and joint aches, fatigue, nausea, and dizziness. These often progressed to bloody diarrhea, severe vomiting, and bleeding from the nose, mouth, and anus. The initial transmission was believed to be due to reuse of the needle for Lokela’s injection without sterilization. Subsequent transmission was also due to care of the sick patients without barrier nursing and the traditional burial preparation method, which involved washing and gastrointestinal tract cleansing.

Two nuns working in Yambuku as nurses also died in the same outbreak.

Sudan ebolavirus
Known human cases and deaths during outbreaks of Sudan Ebolavirus between 1976 and 2003
Known human cases and deaths during outbreaks of Sudan Ebolavirus between 1976 and 2003

Sudan Ebolavirus was the second strand of Ebola reported in 1976. It apparently originated amongst cotton factory workers in Nzara, Sudan. The first case reported was a worker exposed to a potential natural reservoir at the cotton factory. Scientists tested all animals and insects in response to this, however none tested positive for the virus. The carrier is still unknown.

A second case involved a nightclub owner in Nzara, Sudan. The local hospital, Maridi, tested and attempted to treat the patient; however, nothing was successful, and he died. The hospital did not advocate safe and practical procedures in sterilizing and disinfecting the medical tools used on the nightclub owner, likely facilitating the spread of the virus in the hospital.

The most recent outbreak of Sudan Ebolavirus occurred in May 2004. As of May 2004, 20 cases of Sudan Ebolavirus were reported in Yambio County, Sudan, with 5 deaths resulting. The Centers for Disease Control and Prevention confirmed the virus a few days later. The neighbouring countries of Uganda and the Democratic Republic of Congo have increased surveillance in bordering areas, and other similar measures have been taken to control the outbreak. The average fatality rates for Sudan Ebolavirus were 54% in 1976, 68% in 1979, and 53% in 2000/2001. The average case-fatality rate is 54%.

First discovered in November 1989 in a group of 100 Crab-eating macaques (Macaca fascicularis) imported from the Philippines to Reston, Virginia. A parallel infected shipment was also sent to Philadelphia. This strain was highly lethal in monkeys, but did not cause any fatalities in humans. Six of the Reston primate handlers tested positive for the virus, two due to previous exposure. The bio-thriller The Hot Zone was based on this incident.

Further Reston Ebolavirus infected monkeys were shipped again to Reston, and Alice, Texas, in February of 1990. More Reston Ebolavirus infected monkeys were discovered in 1992 in Siena, Italy and in Texas again in March 1996. A high rate of co-infection with Simian hemorragic fever (SHF) was present in all infected monkeys. No human illness has resulted from these two outbreaks.

This subtype of Ebola was first discovered amongst chimpanzees of the Tai Forest in Côte d’Ivoire, Africa. On November 1, 1994, the corpses of two chimpanzees were found in the forest. Necropsies showed blood within the heart to be liquid and brown, no obvious marks seen on the organs, and one presented lungs filled with liquid blood. Studies of tissues taken from the chimps showed results similar to human cases during the 1976 Ebola outbreaks in Zaïre and Sudan. Later in 1994, more dead chimpanzees were discovered, with many testing positive to Ebola using molecular techniques. The source of contamination was believed to be the meat of infected Western Red Colobus monkeys, upon which the chimpanzees preyed.

One of the scientists performing the necropsies on the infected chimpanzees contracted Ebola. She developed symptoms similar to dengue fever approximately a week after the necropsy and was transported to Switzerland for treatment. After two weeks she was discharged from hospital, and was fully recovered six weeks after the infection.

On November 24, 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the Bundibugyo District. After confirmation of samples tested by the United States National Reference Laboratories and the Centers for Disease Control, the World Health Organization has confirmed the presence of a new species of the Ebola virus. On February 20, 2008, the Uganda Ministry officially announced the end of the epidemic in Bundibugyo with the last infected person discharged on January 8, 2008.[9] Ugandan officials confirmed a total of 149 cases of this new Ebola species, with 37 deaths attributed to the strain.

Transmission
Among humans, the virus is transmitted by direct contact with infected body fluids, or to a lesser extent, skin or mucous membrane contact. The incubation period can be anywhere from 2 to 21 days, but is generally between 5 and 10 days.

Although airborne transmission between monkeys has been demonstrated by an accidental outbreak in a laboratory located in Virginia, USA, there is very limited evidence for human-to-human airborne transmission in any reported epidemics. Nurse Mayinga might represent the only possible case. The means by which she contracted the virus remains uncertain.

The infection of human cases with Ebola virus has been documented through the handling of infected chimpanzees, gorillas, and forest antelopes–both dead and alive–as was documented in Côte d’Ivoire, the Republic of Congo and Gabon. The transmission of the Ebola Reston strain through the handling of cynomolgus monkeys has also been reported.

So far, all epidemics of Ebola have occurred in sub-optimal hospital conditions, where practices of basic hygiene and sanitation are often either luxuries or unknown to caretakers and where disposable needles and autoclaves are unavailable or too expensive. In modern hospitals with disposable needles and knowledge of basic hygiene and barrier nursing techniques, Ebola has never spread on such a large scale.

In the early stages, Ebola may not be highly contagious. Contact with someone in early stages may not even transmit the disease. As the illness progresses, bodily fluids from diarrhea, vomiting, and bleeding represent an extreme biohazard. Due to lack of proper equipment and hygienic practices, large scale epidemics occur mostly in poor, isolated areas without modern hospitals or well-educated medical staff. Many areas where the infectious reservoir exists have just these characteristics. In such environments, all that can be done is to immediately cease all needle-sharing or use without adequate sterilization procedures, to isolate patients, and to observe strict barrier nursing procedures with the use of a medical rated disposable face mask, gloves, goggles, and a gown at all times. This should be strictly enforced for all medical personnel and visitors.

Ebola is unlikely to develop(sometimes) into a pandemic, or world-wide infection, due to its difficulty in spreading by airborne transmission and the period of time that the virus can use a living and contagious victim to spread compared to other infectious diseases. In isolated settings such as a quarantined hospital or a remote village, most victims are infected shortly after the first case of infection is present. In addition, the quick onset of symptoms from the time the disease becomes contagious in an individual makes it easy to identify sick individuals and limits an individual’s ability to spread the disease by traveling. Because bodies of the deceased are still infectious, many doctors implemented measures to properly dispose of dead bodies in spite of some traditional local burial rituals.

Antiretroviral drug treatment guidelines have changed over time. Prior to 1987, no antiretroviral drugs were available and treatment consisted of treating complications from the immunodeficiency. After antiretroviral medications were introduced, most clinicians agreed that HIV positive patients with low CD4 counts should be treated, but no consensus formed as to whether to treat patients with high CD4 counts.

In 1995, David Ho promoted a “hit hard, hit early” approach with aggressive treatment with multiple antiretrovirals early in the course of the infection. Later reviews noted that this approach of “hit hard, hit early” ran significant risks of increasing side effects and development of multidrug resistance, and this approach was largely abandoned.

The timing of when to initiate therapy has continued to be a core controversy within the medical community. The development of a stable consensus is hampered by the lack of randomized controlled studies with many guidelines and consensus statements basing their recommendations on observational studies. More recently, the trend has been in favor of earlier treatment of asymptomatic HIV patients, with more studies analyzing various treatment regimens in progress.

There is a consensus among experts that, once initiated, antiretroviral therapy should never be stopped. This is because the selection pressure of incomplete suppression of viral replication in the presence of drug therapy causes the more drug sensitive strains to be selectively inhibited. This allows the drug resistant strains to become dominant. This in turn makes it harder to treat the infected individual as well as anyone else they infect

Current guidelines

The current guidelines use new criteria to consider starting HAART, as described below. However, there remain a range of views on this subject and the decision of whether to commence treatment ultimately rests with the patient and their doctor.

The current guidelines for antiretroviral therapy (ART) from the World Health Organization reflect the 2003 changes to the guidelines and recommend that in resource-limited settings (that is, developing nations), HIV-infected adults and adolescents should start ART when HIV infection has been confirmed and one of the following conditions is present :

• Clinically advanced HIV disease;
• WHO Stage IV HIV disease, irrespective of the CD4 cell count;
• WHO Stage III disease with consideration of using CD4 cell counts less than 350/µl to assist decision making;
• WHO Stage I or II HIV disease with CD4 cell counts less than 200/µl.

The treatment guidelines specifically for the USA are set by the United States Department of Health and Human Services (DHHS). The current guidelines for adults and adolescents were stated on December 1, 2009.

• Antiretroviral therapy should be initiated in all patients with a history of an AIDS-defining illness or with a CD4 count <350 cells/mm3 (AI).

• Antiretroviral therapy should also be initiated, regardless of CD4 count, in patients with the following conditions: pregnancy (AI), HIV- associated nephropathy (AII), and hepatitis B virus (HBV) coinfection when treatment of HBV is indicated (AIII).

• Antiretroviral therapy is recommended for patients with CD4 counts between 350 and 500 cells/mm3. The Panel was divided on the strength of this recommendation: 55% voted for strong recommendation (A) and 45% voted for moderate recommendation (B) (A/B-II).

• For patients with CD4 counts >500 cells/mm3, the Panel was evenly divided: 50% favor starting antiretroviral therapy at this stage of HIV disease (B); 50% view initiating therapy at this stage as optional (C) (B/C-III).

• Patients initiating antiretroviral therapy should be willing and able to commit to lifelong treatment and should understand the benefits and risks of therapy and the importance of adherence (AIII). Patients may choose to postpone therapy, and providers, on a case-by-case basis, may elect to defer therapy based on clinical and/or psychosocial factors.

Rating of Recommendations: A = Strong; B = Moderate; C = Optional Rating of Evidence: I = data from randomized controlled trials; II = data from well-designed nonrandomized trials or observational cohort studies with long-term clinical outcomes; III = expert opinion

Baseline resistance

In countries with a high rate of baseline resistance, resistance testing is recommended prior to starting treatment; or, if the initiation of treatment is urgent, then a “best guess” treatment regimen should be started, which is then modified on the basis of resistance testing. In the UK, there is 11.8% medium to high-level resistance at baseline to the combination of efavirenz + zidovudine + lamivudine, and 6.4% medium to high level resistance to stavudine + lamivudine + nevirapine.

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Updated 29.05.2010

Infectious pathologies are usually qualified as contagious diseases (also called communicable diseases) due to their potentiality of transmission from one person or species to another. Transmission of an infectious disease may occur through one or more of diverse pathways including physical contact with infected individuals. These infecting agents may also be transmitted through liquids, food, body fluids, contaminated objects, airborne inhalation, or through vector-borne spread.

The term infectivity describes the ability of an organism to enter, survive and multiply in the host, while the infectiousness of a disease indicates the comparative ease with which the disease is transmitted to other hosts.An infection however, is not synonymous with an infectious disease, as an infection may not cause important clinical symptoms or impair host function.

Classification
Among the almost infinite varieties of microorganisms, relatively few cause disease in otherwise healthy individuals. Infectious disease results from the interplay between those few pathogens and the defenses of the hosts they infect. The appearance and severity of disease resulting from any pathogen depends upon the ability of that pathogen to damage the host as well as the ability of the host to resist the pathogen. Infectious microorganisms, or microbes, are therefore classified as either primary pathogens or as opportunistic pathogens according to the status of host defenses.

Primary pathogens cause disease as a result of their presence or activity within the normal, healthy host, and their intrinsic virulence (the severity of the disease they cause) is, in part, a necessary consequence of their need to reproduce and spread. Many of the most common primary pathogens of humans only infect humans, however many serious diseases are caused by organisms acquired from the environment or which infect non-human hosts.

Organisms which cause an infectious disease in a host with depressed resistance are classified as opportunistic pathogens. Opportunistic disease may be caused by microbes that are ordinarily in contact with the host, such as bacteria or fungi in the gastrointestinal or the upper respiratory tract, and they may also result from (otherwise innocuous) microbes acquired from other hosts (as in Clostridium difficile enterocolitis) or from the environment as a result of traumatic introduction (as in surgical wound infections or compound fractures). An opportunistic disease requires impairment of host defenses, which may occur as a result of genetic defects (such as Chronic granulomatous disease), exposure to antimicrobial drugs or immunosuppressive chemicals (as might occur following poisoning or cancer chemotherapy), exposure to ionizing radiation, or as a result of an infectious disease with immunosuppressive activity (such as with measles, malaria or HIV disease). Primary pathogens may also cause more severe disease in a host with depressed resistance than would normally occur in an immunosufficient host.

One way of proving that a given disease is “infectious”, is to satisfy Koch’s postulates (first proposed by Robert Koch), which demands that the infectious agent be identified only in patients and not in healthy controls, and that patients who contract the agent also develop the disease. These postulates were first used in the discovery that Mycobacteria species cause tuberculosis. Koch’s postulates cannot be met ethically for many human diseases because they require experimental infection of a healthy individual with a pathogen produced as a pure culture. Often, even diseases that are quite clearly infectious do not meet the infectious criteria. For example, Treponema pallidum, the causative spirochete of syphilis, cannot be cultured in vitro – however the organism can be cultured in rabbit testes. It is less clear that a pure culture comes from an animal source serving as host than it is when derived from microbes derived from plate culture. Epidemiology is another important tool used to study disease in a population. For infectious diseases it helps to determine if a disease outbreak is sporadic (occasional occurrence), endemic (regular cases often occurring in a region), epidemic (an unusually high number of cases in a region), or pandemic (a global epidemic).

Transmission
An infectious disease is transmitted from some source. Defining the means of transmission plays an important part in understanding the biology of an infectious agent, and in addressing the disease it causes. Transmission may occur through several different mechanisms. Respiratory diseases and meningitis are commonly acquired by contact with aerosolized droplets, spread by sneezing, coughing, talking or even singing. Gastrointestinal diseases are often acquired by ingesting contaminated food and water. Sexually transmitted diseases are acquired through contact with bodily fluids, generally as a result of sexual activity. Some infectious agents may be spread as a result of contact with a contaminated, inanimate object (known as a fomite), such as a coin passed from one person to another, while other diseases penetrate the skin directly.

Transmission of infectious diseases may also involve a “vector”. Vectors may be mechanical or biological. A mechanical vector picks up an infectious agent on the outside of its body and transmits it in a passive manner. An example of a mechanical vector is a housefly, which lands on cow dung, contaminating its appendages with bacteria from the feces, and then lands on food prior to consumption. The pathogen never enters the body of the fly.

In contrast, biological vectors harbor pathogens within their bodies and deliver pathogens to new hosts in an active manner, usually a bite. Biological vectors are often responsible for serious blood-borne diseases, such as malaria, viral encephalitis, Chagas disease and African sleeping sickness. Biological vectors are usually, though not exclusively, arthropods, such as mosquitoes, ticks, fleas and lice. Vectors are often required in the life cycle of a pathogen. A common strategy, used to control vector borne infectious diseases, is to interrupt the life cycle of a pathogen, by killing the vector.

The relationship between virulence and transmission is complex, and has important consequences for the long term evolution of a pathogen. Since it takes time for a microbe and a new host species to co-evolve, an emerging pathogen may hit its earliest victims especially hard. It is usually in the first wave of a new disease that death rates are highest. If a disease is rapidly fatal, the host may die before the microbe can get passed along to another host. However, this cost may be overwhelmed by the short term benefit of higher infectiousness if transmission is linked to virulence, as it is for instance in the case of cholera (the explosive diarrhea aids the bacterium in finding new hosts) or many respiratory infections (sneezing and coughing create infectious aerosols).

Diagnosis and therapy
Diagnosis of infectious disease sometimes involves identifying an infectious agent either directly or indirectly. In practice most minor infectious diseases such as warts, cutaneous abscesses, respiratory system infections and diarrheal diseases are diagnosed by their clinical presentation. Conclusions about the cause of the disease are based upon the likelihood that a patient came in contact with a particular agent, the presence of a microbe in a community, and other epidemiological considerations. Given sufficient effort, all known infectious agents can be specifically identified.

The benefits of identification, however, are often greatly outweighed by the cost, as often there is no specific treatment, the cause is obvious, or the outcome of an infection is benign.
Specific identification of an infectious agent is usually only determined when such identification can aid in the treatment or prevention of the disease, or to advance knowledge of the course of an illness prior to the development of effective therapeutic or preventative measures. For example, in the early 1980s, prior to the appearance AZT for the treatment of AIDS, the course of the disease was closely followed by monitoring the composition of patient blood samples, even though the outcome would not offer the patient any further treatment options. In part, these studies on the appearance of HIV in specific communities permitted the advancement of hypotheses as to the route of transmission of the virus. By understanding how the disease was transmitted, resources could be targeted to the communities at greatest risk in campaigns aimed at reducing the number of new infections.

The specific serological diagnostic identification, and later genotypic or molecular identification, of HIV also enabled the development of hypotheses as to the temporal and geographical origins of the virus, as well as a myriad of other hypothesis. The development of molecular diagnostic tools have enabled physicians and researchers to monitor the efficacy of treatment with anti-retroviral drugs. Molecular diagnostics are now commonly used to identify HIV in healthy people long before the onset of illness and have been used to demonstrate the existence of people who are genetically resistant to HIV infection. Thus, while there still is no cure for AIDS, there is great therapeutic and predictive benefit to identifying the virus and monitoring the virus levels within the blood of infected indiviuals, both for the patient and for the community at large.

Methods of Diagnosis

Diagnosis of infectious disease is nearly always initiated by medical history and physical examination. More detailed identification techniques involve the culture of infectious agents isolated from a patient. Culture allows identification of infectious organisms by examining their microscopic features, by detecting the presence of substances produced by pathogens, and by directly identifying an organism by its genotype. Other techniques (such as X-rays, CT scans, PET scans or NMR) are used to produce images of internal abnormalities resulting from the growth of an infectious agent. The images are useful in detection of, for example, a bone abscess or a spongiform encephalopathy produced by a prion.

Microbiological culture is a principal tool used to diagnose infectious disease. In a microbial culture, a growth medium is provided for a specific agent. A sample taken from potentially diseased tissue or fluid is then tested for the presence of an infectious agent able to grow within that medium. Most pathogenic bacteria are easily grown on nutrient agar, a form of solid medium that supplies carbohydrates and proteins necessary for growth of a bacterium, along with copious amounts of water. A single bacterium will grow into a visible mound on the surface of the plate called a colony, which may be separated from other colonies or melded together into a “lawn”. The size, color, shape and form of a colony is characteristic of the bacterial species, its specific genetic makeup (its strain), and the environment which supports its growth. Other ingredients are often added to the plate to aid in identification. Plates may contain substances that permit the growth of some bacteria and not others, or that change color in response to certain bacteria and not others. Bacteriological plates such as these are commonly used in the clinical identification of infectious bacteria. Microbial culture may also be used in the identification of viruses: the medium in this case being cells grown in culture that the virus can infect, and then alter or kill. In the case of viral identification, a region of dead cells results from viral growth, and is called a “plaque”. Eukaryoticparasites may also be grown in culture as a means of identifying a particular agent.

In the absence of suitable plate culture techniques, some microbes require culture within live animals. Bacteria such as Mycobacterium leprae and T. pallidum can be grown in animals, although serological and microscopic techniques make the use of live animals unnecessary. Viruses are also usually identified using alternatives to growth in culture or animals. Some viruses may be grown in embryonated eggs. Another useful identification method is Xenodiagnosis, or the use of a vector to support the growth of an infectious agent. Chagas disease is the most significant example, because it is difficult to directly demonstrate the presence of the causative agent, Trypanosoma cruzi in a patient, which therefore makes it difficult to definitively make a diagnosis. In this case, xenodiagnosis involves the use of the vector of the Chaga’s agent T. cruzi, an uninfected triatomine bug (subfamily Triatominae), which takes a blood meal from a person suspected of having been infected. The bug is later inspected for growth of T. cruzi within its gut.

Microscopy

Another principle tool in the diagnosis of infectious disease is microscopy. Virtually all of the culture techniques discussed above rely, at some point, on microscopic examination for definitive identification of the infectious agent. Microscopy may be carried out with simple instruments, such as the compound light microscope, or with instruments as complex as an electron microscope. Samples obtained from patients may be viewed directly under the light microscope, and can often rapidly lead to identification. Microscopy is often also used in conjunction with biochemical staining techniques, and can be made exquisitely specific when used in combination with antibodybased techniques. For example, the use of antibodies made artificially fluorescent (fluorescently labeled antibodies) can be directed to bind to and identify a specific antigenspresent on a pathogen. A fluorescence microscope is then used to detect fluorescently labeled antibodies bound to internalized antigens within clinical samples or cultured cells. This technique is especially useful in the diagnosis of viral diseases, where the light microscope is incapable of identifying a virus directly.

Other microscopic procedures may also aid in identifying infectious agents. Almost all cells readily stain with a number of basic dyes due to the electrostatic attraction between negatively charged cellular molecules and the positive charge on the dye. A cell is normally transparent under a microscope, and using a stain increases the contrast of a cell with its background. Staining a cell with a dye such as Giemsa stain or crystal violet allows a microscopist to describe its size, shape, internal and external components and its associations with other cells. The response of bacteria to different staining procedures is used in the taxonomic classification of microbes as well. Two methods, the Gram stain and the acid-fast stain, are the standard approaches used to classify bacteria and to diagnosis of disease. The Gram stain identifies the bacterial groups Firmicutes and Actinobacteria, both of which contain many significant human pathogens. The acid-fast staining procedure identifies the Actinobacterial genera Mycobacterium and Nocardia.

Biochemical tests

Biochemical tests used in the identification of infectious agents include the detection of metabolic or enzymatic products characteristic of a particular infectious agent. Since bacteria ferment carbohydrates in patterns characteristic of their genus and species, the detection of fermentation products is commonly used in bacterial identification. Acids, alcohols and gases are usually detected in these tests when bacteria are grown in selective liquid or solid media.

The isolation of enzymes from infected tissue can also provide the basis of a biochemical diagnosis of an infectious disease. For example, humans can make neither RNA replicases nor reverse transcriptase, and the presence of these enzymes are characteristic of specific types of viral infections. The ability of the viral protein hemagglutinin to bind red blood cells together into a detectable matrix may also be characterized as a biochemical test for viral infection, although strictly speaking hemagglutinin is not an enzyme and has no metabolic function.

Serological methods are highly sensitive, specific and often extremely rapid tests used to identify microorganisms. These tests are based upon the ability of an antibody to bind specifically to an antigen. The antigen, usually a protein or carbohydrate made by an infectious agent, is bound by the antibody. This binding then sets off a chain of events that can be visibly obvious in various ways, dependent upon the test. For example, “Strep throat” is often diagnosed within minutes, and is based on the appearance of antigens made by the causative agent, Streptococcus pyogenes, that is retrieved from a patients throat with a cotton swab. Serological tests, if available, are usually the preferred route of identification, however the tests are costly to develop and the reagents used in the test often require refrigeration. Some serological methods are extremely costly, although when commonly used, such as with the “strep test”, they can be inexpensive.

Molecular diagnostics

Technologies based upon the polymerase chain reaction (PCR) will become nearly ubiquitous gold standards of diagnostics of the near future, for several reasons. First, the catalog of infectious agents has grown to the point that virtually all of the significant infectious agents of the human population have been identified. Second, an infectious agent must grow within the human body to cause disease; essentially it must amplify its own nucleic acids in order to cause a disease. This amplification nucleic acid in infected tissue offers an opportunity to detect the infectious agent by using PCR. Third, the essential tools for generating PCR (primers) are defined by the genomes of the infectious agents, and with time those genomes will be known, if they are not already.

Thus, the technological ability to detect any infectious agent rapidly and specifically are currently available. The only remaining blockades to the use of PCR as a standard tool of diagnosis are in its cost and application, neither of which is insurmountable. The diagnosis of a few diseases will not benefit from the development of PCR methods, such as some of the clostridial diseases (tetanus and botulism). These diseases are fundamentally biological poisonings by relatively small numbers of infectious bacteria that produce extremely potent neurotoxins. A significant proliferation of the infectious agent does not occur, this limits the ability of PCR to detect the presence of any bacteria.

The study of infectious disease

History

Abū Alī ibn Sīnā (Avicenna) discovered the contagious nature of infectious diseases in the early 11th century, for which he is considered the father of modern medicine. He introduced quarantine as a means of limiting the spread of contagious and infectious diseases in The Canon of Medicine, circa 1020. He also stated that bodily secretion is contaminated by foul foreign earthly bodies before being infected, but he did not view them as primary causes of disease.

When the Black Death bubonic plague reached al-Andalus in the 14th century, Ibn Khatima and Ibn al-Khatib hypothesized that infectious diseases are caused by microorganisms which enter the human body. Such ideas became more popular in Europe during the renaissance, particularly through the writing of the Italian monk Girolamo Fracastoro.

Anton van Leeuwenhoek (1632-1723) advanced the science of microscopy, allowing for easy visualization of bacteria.

Louis Pasteur proved beyond doubt that certain diseases are caused by infectious agents, and developed a vaccine for rabies.

Robert Koch, provided the study of infectious diseases with a scientific basis known as Koch’s postulates.

Edward Jenner, Jonas Salk and Albert Sabin developed effective vaccines for smallpox and polio, which would later result in the eradication and near-eradication of these diseases, respectively.

Alexander Fleming discovered the world’s first antibiotic Penicillin.

Gerhard Domagk develops Sulphonamides, the first broad spectrum synthetic antibacterial drugs.

Medical specialists

The medical treatment of infectious diseases falls into the medical field of Infectiology and in some cases the study of propagation pertains to the field of Epidemiology. Generally, infections are initially diagnosed by primary care physicians or internal medicine specialists. For example, an “uncomplicated” pneumonia will generally be treated by the internist or the pulmonologist (lung physician).The work of the infectiologist therefore entails working with both patients and general practitioners, as well as laboratory scientists, immunologists, bacteriologists and other specialists..

An infectious disease team may be alerted when:

• The disease has not been definitively diagnosed after an initial workup
• The patient is immunocompromised (for example, in AIDS or after chemotherapy);
• The infectious agent is of an uncommon nature (e.g. tropical diseases);
• The disease has not responded to first line antibiotics;
• The disease might be dangerous to other patients, and the patient might have to be isolated.

Source: Wiki

In 1975 the United Nations Children’s Fund, the United Nations Development Programme, the World Bank and the World Health Organization established the Special Programme for Research and Training in Tropical Diseases (TDR) to focus on neglected infectious diseases which disproportionately affect poor and marginalized populations in developing regions of Africa, Asia, Central America and South America. The current TDR disease portfolio includes the following entries:

• Chagas disease

  (also called American trypanosomiasis) is a parasitic disease which occurs in the Americas, particularly in South America. Its pathogenic agent is a flagellate protozoan named Trypanosoma cruzi, which istransmitted mostly by blood-sucking assassin bugs, however other methods of transmission are possible, such as ingestion of food contaminated with parasites, blood transfusion and fetal transmission. Between 16 and 18 million people are currently infected.^[6]

• Dengue
• Helminths
• African trypanosomiasis

  or sleeping sickness, is a parasitic disease, caused by protozoa called trypansomes. The two responsible for African trypanosomiasis are Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense.These parasites are transmitted by the tsetse fly

• Leishmaniasis

  caused by protozoan parasites of the genus Leishmania, and transmitted by the bite of certain species of sand fly.

• Leprosy^†

  (or Hansen’s disease) is a chronic infectious disease caused by Mycobacterium leprae. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes. Contrary to popular conception, leprosy does not cause body parts to simply fall off, and it differs from tzaraath, the malady described in the Hebrew scriptures and previously translated into English as leprosy.

• Lymphatic filariasis

  is a parasitic disease caused by thread-like parasitic filarial worms called nematode worms, all transmitted by mosquitoes. Loa loa is another filarial parasite transmitted by the deer fly. 120 million people are infected worldwide. It is carried by over half the population in the most severe endemic areas.  The most noticeable symptom is elephantiasis: a thickening of the skin and underlying tissues. Elephantiasis is caused by chronic infection by filarial worms in the lymph nodes. This clogs the lymph nodes and slows the draining of lymph fluid from a portion of the body.

• Malaria

  Caused by a Protozoan parasites transmitted by female Anopheles mosquitoes, as they are the blood-feeders. The disease is caused by species of the genus Plasmodium. Malaria infects 300-500 million people each year, killing more than 1 million.

• Onchocerciasis

  (pronounced /ɒŋkoʊsɜrˈsaɪ.əsɪs/) or river blindness is the world’s second leading infectious cause of blindness. It is caused by Onchocerca volvulus, a parasitic worm. It is transmitted through the bite of a black fly. The worms spread throughout the body, and when they die, they cause intense itching and a strong immune system response that can destroy nearby tissue, such as the eye. About 18 million people are currently infected with this parasite. Approximately 300,000 have been irreversibly blinded by it.

• Schistosomiasis

  (pronounced /ˌʃɪstoʊsɵˈmaɪ.əsɪs/) also known as schisto or snail fever, is a parasitic disease caused by several species of flatworm in areas with freshwater snails, which may carry the parasite. The most common form of transmission is by wading or swimming in lakes, ponds and other bodies of water containing the snails and the parasite. More than 200 million people worldwide are infected by schistosomiasis.

• Sexually transmitted infections
• TB/HIV coinfection
• Tuberculosis^†

  (abbreviated as TB), is a bacterial infection of the lungs or other tissues, which is highly prevalent in the world, with mortality over 50% if untreated. It is a communicable disease, transmitted by aerosolexpectorant from a cough, sneeze, speak, kiss, or spit. Over one-third of the world’s population has been infected by the TB bacterium.

Some of the strategies for controlling tropical diseases include:

• Draining wetlands to reduce populations of insects and other vectors.
• The application of insecticides and/or insect repellents) to strategic surfaces such as: clothing, skin, buildings, insect habitats, and bed nets.
• The use of a mosquito net over a bed (also known as a “bed net”) to reduce nighttime transmission, since certain species of tropical mosquitoes feed mainly at night.
• Use of water wells, and/or water filtration, water filters, or water treatment with water tablets to produce drinking water free of parasites.
• Development and use of vaccines to promote disease immunity.
• Pharmacologic pre-exposure prophylaxis (to prevent disease before exposure to the environment and/or vector).
• Pharmacologic post-exposure prophylaxis (to prevent disease after exposure to the environment and/or vector).
• Pharmacologic treatment (to treat disease after infection or infestation).
• Assisting with economic development in endemic regions. For example by providing microloans to enable investments in more efficient and productive agriculture. This in turn can help subsistence farming to become more profitable, and these profits can be used by local populations for disease prevention and treatment, with the added benefit of reducing the poverty rate.

Source: Wiki

Nanotechnology is a highly multidisciplinary field, drawing from fields such as applied physics, materials science, interface and colloid science, device physics, supramolecular chemistry (which refers to the area of chemistry that focuses on the noncovalent bonding interactions of molecules), self-replicating machines and robotics, chemical engineering, mechanical engineering, biological engineering, and electrical engineering. Grouping of the sciences under the umbrella of “nanotechnology” has been questioned on the basis that there is little actual boundary-crossing between the sciences that operate on the nano-scale. Instrumentation is the only area of technology common to all disciplines; on the contrary, for example pharmaceutical and semiconductor industries do not “talk with each other”. Corporations that call their products “nanotechnology” typically market them only to a certain industrial cluster.


Two main approaches are used in nanotechnology. In the “bottom-up” approach, materials and devices are built from molecular components which assemble themselves chemically by principles of molecular recognition. In the “top-down” approach, nano-objects are constructed from larger entities without atomic-level control. The impetus for nanotechnology comes from a renewed interest in Interface and Colloid Science, coupled with a new generation of analytical tools such as the atomic force microscope (AFM), and the scanning tunneling microscope (STM). Combined with refined processes such as electron beam lithography and molecular beam epitaxy, these instruments allow the deliberate manipulation of nanostructures, and lead to the observation of novel phenomena.

Examples of nanotechnology are the manufacture of polymers based on molecular structure, and the design of computer chip layouts based on surface science. Despite the promise of nanotechnologies such as quantum dots and nanotubes, real commercial applications have mainly used the advantages of colloidal nanoparticles in bulk form, such as suntan lotion, cosmetics, protective coatings, drug delivery, and stain resistant clothing.

The first use of the concepts in ‘nano-technology’ (but predating use of that name) was in “There’s Plenty of Room at the Bottom,” a talk given by physicist Richard Feynman at an American Physical Society meeting at Caltech on December 29, 1959. Feynman described a process by which the ability to manipulate individual atoms and molecules might be developed, using one set of precise tools to build and operate another proportionally smaller set, so on down to the needed scale. In the course of this, he noted, scaling issues would arise from the changing magnitude of various physical phenomena: gravity would become less important, surface tension and Van der Waals attraction would become more important, etc. This basic idea appears plausible, and exponential assembly enhances it with parallelism to produce a useful quantity of end products.

The term “nanotechnology” was defined by Tokyo Science University Professor Norio Taniguchi in a 1974 paper[3] as follows: “‘Nano-technology’ mainly consists of the processing of, separation, consolidation, and deformation of materials by one atom or by one molecule.” In the 1980s the basic idea of this definition was explored in much more depth by Dr. K. Eric Drexler, who promoted the technological significance of nano-scale phenomena and devices through speeches and the books Engines of Creation: The Coming Era of Nanotechnology (1986) and Nanosystems: Molecular Machinery, Manufacturing, and Computation, and so the term acquired its current sense. Engines of Creation: The Coming Era of Nanotechnology is considered the first book on the topic of nanotechnology. Nanotechnology and nanoscience got started in the early 1980s with two major developments; the birth of cluster science and the invention of the scanning tunneling microscope (STM).

This development led to the discovery of fullerenes in 1986 and carbon nanotubes a few years later. In another development, the synthesis and properties of semiconductor nanocrystals was studied; This led to a fast increasing number of metal oxide nanoparticles of quantum dots. The atomic force microscope was invented six years after the STM was invented. In 2000, the United States National Nanotechnology Initiative was founded to coordinate Federal nanotechnology research and development.

One nanometer (nm) is one billionth, or 10-9 of a meter. To put that scale in context, the comparative size of a nanometer to a meter is the same as that of a marble to the size of the earth.[5] Or another way of putting it: a nanometer is the amount a man’s beard grows in the time it takes him to raise the razor to his face.[5]

Typical carbon-carbon bond lengths, or the spacing between these atoms in a molecule, are in the range 0.12-0.15 nm, and a DNA double-helix has a diameter around 2 nm. On the other hand, the smallest cellular lifeforms, the bacteria of the genus Mycoplasma, are around 200 nm in length.

Larger to smaller: a materials perspective
A number of physical phenomena become pronounced as the size of the system decreases. These include statistical mechanical effects, as well as quantum mechanical effects, for example the “quantum size effect” where the electronic properties of solids are altered with great reductions in particle size. This effect does not come into play by going from macro to micro dimensions. However, it becomes dominant when the nanometer size range is reached. Additionally, a number of physical (mechanical, electrical, optical, etc.) properties change when compared to macroscopic systems. One example is the increase in surface area to volume ratio altering mechanical, thermal and catalytic properties of materials. Novel mechanical properties of nanosystems are of interest in the nanomechanics research. The catalytic activity of nanomaterials also opens potential risks in their interaction with biomaterials.

Materials reduced to the nanoscale can show different properties compared to what they exhibit on a macroscale, enabling unique applications. For instance, opaque substances become transparent (copper); inert materials become catalysts (platinum); stable materials turn combustible (aluminum); solids turn into liquids at room temperature (gold); insulators become conductors (silicon). A material such as gold, which is chemically inert at normal scales, can serve as a potent chemical catalyst at nanoscales. Much of the fascination with nanotechnology stems from these quantum and surface phenomena that matter exhibits at the nanoscale.

Simple to complex: a molecular perspective
Modern synthetic chemistry has reached the point where it is possible to prepare small molecules to almost any structure. These methods are used today to produce a wide variety of useful chemicals such as pharmaceuticals or commercial polymers. This ability raises the question of extending this kind of control to the next-larger level, seeking methods to assemble these single molecules into supramolecular assemblies consisting of many molecules arranged in a well defined manner.

These approaches utilize the concepts of molecular self-assembly and/or supramolecular chemistry to automatically arrange themselves into some useful conformation through a bottom-up approach. The concept of molecular recognition is especially important: molecules can be designed so that a specific conformation or arrangement is favored due to non-covalent intermolecular forces. The Watson-Crick basepairing rules are a direct result of this, as is the specificity of an enzyme being targeted to a single substrate, or the specific folding of the protein itself. Thus, two or more components can be designed to be complementary and mutually attractive so that they make a more complex and useful whole.

Such bottom-up approaches should be able to produce devices in parallel and much cheaper than top-down methods, but could potentially be overwhelmed as the size and complexity of the desired assembly increases. Most useful structures require complex and thermodynamically unlikely arrangements of atoms. Nevertheless, there are many examples of self-assembly based on molecular recognition in biology, most notably Watson-Crick basepairing and enzyme-substrate interactions. The challenge for nanotechnology is whether these principles can be used to engineer novel constructs in addition to natural ones.

Molecular nanotechnology: a long-term view
Molecular nanotechnology, sometimes called molecular manufacturing, is a term given to the concept of engineered nanosystems (nanoscale machines) operating on the molecular scale. It is especially associated with the concept of a molecular assembler, a machine that can produce a desired structure or device atom-by-atom using the principles of mechanosynthesis. Manufacturing in the context of productive nanosystems is not related to, and should be clearly distinguished from, the conventional technologies used to manufacture nanomaterials such as carbon nanotubes and nanoparticles.

When the term “nanotechnology” was independently coined and popularized by Eric Drexler (who at the time was unaware of an earlier usage by Norio Taniguchi) it referred to a future manufacturing technology based on molecular machine systems. The premise was that molecular-scale biological analogies of traditional machine components demonstrated molecular machines were possible: by the countless examples found in biology, it is known that sophisticated, stochastically optimised biological machines can be produced.

It is hoped that developments in nanotechnology will make possible their construction by some other means, perhaps using biomimetic principles. However, Drexler and other researchers[6] have proposed that advanced nanotechnology, although perhaps initially implemented by biomimetic means, ultimately could be based on mechanical engineering principles, namely, a manufacturing technology based on the mechanical functionality of these components (such as gears, bearings, motors, and structural members) that would enable programmable, positional assembly to atomic specification (PNAS-1981). The physics and engineering performance of exemplar designs were analyzed in Drexler’s book Nanosystems.

But Drexler’s analysis is very qualitative and does not address very pressing issues, such as the “fat fingers” and “Sticky fingers” problems. In general it is very difficult to assemble devices on the atomic scale, as all one has to position atoms are other atoms of comparable size and stickyness. Another view, put forth by Carlo Montemagno, is that future nanosystems will be hybrids of silicon technology and biological molecular machines. Yet another view, put forward by the late Richard Smalley, is that mechanosynthesis is impossible due to the difficulties in mechanically manipulating individual molecules.

This led to an exchange of letters in the ACS publication Chemical & Engineering News in 2003.Though biology clearly demonstrates that molecular machine systems are possible, non-biological molecular machines are today only in their infancy. Leaders in research on non-biological molecular machines are Dr. Alex Zettl and his colleagues at Lawrence Berkeley Laboratories and UC Berkeley. They have constructed at least three distinct molecular devices whose motion is controlled from the desktop with changing voltage: a nanotube nanomotor, a molecular actuator, and a nanoelectromechanical relaxation oscillator.

An experiment indicating that positional molecular assembly is possible was performed by Ho and Lee at Cornell University in 1999. They used a scanning tunneling microscope to move an individual carbon monoxide molecule (CO) to an individual iron atom (Fe) sitting on a flat silver crystal, and chemically bound the CO to the Fe by applying a voltage.

Applications
As of April 24, 2008 The Project on Emerging Nanotechnologies claims that over 609 nanotech products exist, with new ones hitting the market as a pace of 3-4 a week. The project lists all of the products in a database. Most applications are limited to the use of “first generation” passive nanomaterials which includes titanium dioxide in sunscreen, cosmetics and some food products; silver in food packaging, clothing, disinfectants and household appliances; zinc oxide in sunscreens and cosmetics, surface coatings, paints and outdoor furniture varnishes; and cerium oxide as a fuel catalyst.

The National Science Foundation (a major source of funding for nanotechnology in the United States) funded researcher David Berube to study the field of nanotechnology. His findings are published in the monograph “Nano-Hype: The Truth Behind the Nanotechnology Buzz”. This published study (with a foreword by Mihail Roco, Senior Advisor for Nanotechnology at the National Science Foundation) concludes that much of what is sold as “nanotechnology” is in fact a recasting of straightforward materials science, which is leading to a “nanotech industry built solely on selling nanotubes, nanowires, and the like” which will “end up with a few suppliers selling low margin products in huge volumes.” Further applications which require actual manipulation or arrangement of nanoscale components await further research. Though technologies branded with the term ‘nano’ are sometimes little related to and fall far short of the most ambitious and transformative technological goals of the sort in molecular manufacturing proposals, the term still connotes such ideas. Thus there may be a danger that a “nano bubble” will form, or is forming already, from the use of the term by scientists and entrepreneurs to garner funding, regardless of interest in the transformative possibilities of more ambitious and far-sighted work.

Nanofiltration may come to be an important application, although future research must be careful to investigate possible toxicity.


In 1999, the ultimate CMOS transistor developed at the Laboratory for Electronics and Information Technology in Grenoble, France, tested the limits of the principles of the MOSFET transistor with a diameter of 18 nm (approximately 70 atoms placed side by side). This was almost one tenth the size of the smallest industrial transistor in 2003 (130 nm in 2003, 90 nm in 2004 and 65 nm in 2005). It enabled the theoretical integration of seven billion junctions on a €1 coin. However, the CMOS transistor, which was created in 1999, was not a simple research experiment to study how CMOS technology functions, but rather a demonstration of how this technology functions now that we ourselves are getting ever closer to working on a molecular scale. Today it would be impossible to master the coordinated assembly of a large number of these transistors on a circuit and it would also be impossible to create this on an industrial level.

Cancer

The small size of nanoparticles endows them with properties that can be very useful in oncology, particularly in imaging. Quantum dots (nanoparticles with quantum confinement properties, such as size-tunable light emission), when used in conjunction with MRI (magnetic resonance imaging), can produce exceptional images of tumor sites. These nanoparticles are much brighter than organic dyes and only need one light source for excitation. This means that the use of fluorescent quantum dots could produce a higher contrast image and at a lower cost than today’s organic dyes used as contrast media.


Another nanoproperty, high surface area to volume ratio, allows many functional groups to be attached to a nanoparticle, which can seek out and bind to certain tumor cells. Additionally, the small size of nanoparticles (10 to 100 nanometers), allows them to preferentially accumulate at tumor sites (because tumors lack an effective lymphatic drainage system). A very exciting research question is how to make these imaging nanoparticles do more things for cancer. For instance, is it possible to manufacture multifunctional nanoparticles that would detect, image, and then proceed to treat a tumor? This question is under vigorous investigation; the answer to which could shape the future of cancer treatment. A promising new cancer treatment that may one day replace radiation and chemotherapy is edging closer to human trials. Kanzius RF therapy attaches microscopic nanoparticles to cancer cells and then “cooks” tumors inside the body with radio waves that heat only the nanoparticles and the adjacent (cancerous) cells.

Source Wiki

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[b]Cookies and Other Tracking Technologies[/b]

Some of our Web pages utilize “cookies” and other tracking technologies. A “cookie” is a small text file that may be used, for example, to collect information about Web site activity. Some cookies and other technologies may serve to recall Personal Information previously indicated by a Web user. Most browsers allow you to control cookies, including whether or not to accept them and how to remove them.

You may set most browsers to notify you if you receive a cookie, or you may choose to block cookies with your browser, but please note that if you choose to erase or block your cookies, you will need to re-enter your original user ID and password to gain access to certain parts of the Web site.

Tracking technologies may record information such as Internet domain and host names; Internet protocol (IP) addresses; browser software and operating system types; clickstream patterns; and dates and times that our site is accessed. Our use of cookies and other tracking technologies allows us to improve our Web site and your Web experience. We may also analyze information that does not contain Personal Information for trends and statistics.

Privacy Policy Changes
16/04/2008 updated

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