MTOR inhibitors are a class of drugs that inhibit the mammalian target of rapamycin, a serine/threonine-specific protein kinase that belongs to the family of phosphatidylinositol-3 kinase related kinases. MTOR regulates cellular metabolism and proliferation by forming and signaling through two protein complexes, mTORC1 and mTORC2; the most established mTOR inhibitors are so-called rapalogs, which have shown tumor responses in clinical trials against various tumor types. The discovery of mTOR was made a few decades ago while investigating the mechanism of action of its inhibitor, rapamycin. Rapamycin was first discovered in 1975 in a soil sample from Easter Island of South Pacific known as Rapa Nui, from where its name is derived. Rapamycin is a macrolide, produced by the microorganism Streptomyces hygroscopicus and showed antifungal properties. Shortly after its discovery, immunosuppressive properties were detected, which led to the establishment of rapamycin as an immunosuppressant. In the 1980s, rapamycin was found to have anticancer activity although the exact mechanism of action remained unknown until many years later.
In the 1990s there was a dramatic change in this field due to studies on the mechanism of action of rapamycin and the identification of the drug target. It was found that rapamycin inhibited cellular cell cycle progression. Research on mTOR inhibition has promising results. In general, protein kinases are classified in two major categories based on their substrate specificity, protein tyrosine kinases and protein serine/threonine kinases. Dual-specificity kinases are subclass of the tyrosine kinases.mTOR is a kinase within the family of phosphatidylinositol-3 kinase-related kinases, a family of serine/threonine protein kinases, with a sequence similarity to the family of lipid kinases, PI3Ks. These kinases have different biological functions, but are all large proteins with common domain structure. PIKKs have four domains at the protein level. From the N-terminus to the C-terminus, these domains are named FRAP-ATM-TRAAP, the kinase domain, the PIKK-regulatory domain, the FAT-C-terminal; the FAT domain, consisting of four α-helices, is N-terminal to KD, but that part is referred to as the FKBP12-rapamycin-binding domain, which binds the FKBP12-rapamycin complex.
The FAT domain consists of repeats, referred to as HEAT. Specific protein activators regulate the PIKK kinases but binding of them to the kinase complex causes a conformational change that increases substrate access to the kinase domain. Protein kinases have become popular drug targets, they have been targeted for the discovery and design of small molecule inhibitors and biologics as potential therapeutic agents. Small-molecule inhibitors of protein kinases prevent either phosphorylation of proteins substrates or autophosphorylation of the kinase itself, it appears that growth factors, amino acids, ATP, oxygen levels regulate mTOR signaling. Several downstream pathways that regulate cell-cycle progression, initiation, transcriptional stress responses, protein stability, survival of cells are signaling through mTOR; the serine/threonine kinase mTOR is a downstream effector of the PI3K/AKT pathway, forms two distinct multiprotein complexes, mTORC1 and mTORC2. These two complexes have a separate network of protein partners, feedback loops and regulators.
MTORC1 consists of mTOR and two positive regulatory subunits and mammalian LST8, two negative regulators, proline-rich AKT substrate 40 and DEPTOR. MTORC2 consists of mTOR, mLST8, mSin1, rictor, DEPTOR.mTORC1 is sensitive to rapamycin but mTORC2 is considered to be resistant and is insensitive to nutrients and energy signals. MTORC2 is activated by growth factors, phosphorylates PKCα, AKT and paxillin, regulates the activity of the small GTPase and Rho related to cell survival and regulation of the actin cytoskeleton; the mTORC1 signaling cascade is activated by phosphorylated AKT and results in phosphorylation of S6K1, 4EBP1, which lead to mRNA translation. Many human tumors occur because of dysregulation of mTOR signaling, can confer higher susceptibility to inhibitors of mTOR. Deregulations of multiple elements of the mTOR pathway, like PI3K amplification/mutation, PTEN loss of function, AKT overexpression, S6K1, 4EBP1, eIF4E overexpression have been related to many types of cancers. Therefore, mTOR is an interesting therapeutic target for treating multiple cancers, both the mTOR inhibitors themselves or in combination with inhibitors of other pathways.
Upstream, PI3K/AKT signalling is deregulated through a variety of mechanisms, including overexpression or activation of growth factor receptors, such as HER-2 and IGFR, mutations in PI3K and mutations/amplifications of AKT. Tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 is a negative regulator of PI3K signaling. In many cancers the PTEN expression is decreased and may be downregulated through several mechanisms, including mutations, loss of heterozygosity and protein instability. Downstream, the mTOR effectors S6 kinase 1, eukaryotic initiation factor 4E-binding protein 1 and eukaryotic initiation factor 4E are related to cellular transformation. S6K1 is a key regulator of cell growth and phosphorylates other important targets. Both eIF4E and S6K1 are included in cellular transformation and their overexpressi
A T cell, or T lymphocyte, is a type of lymphocyte that plays a central role in cell-mediated immunity. T cells can be distinguished from other lymphocytes, such as B cells and natural killer cells, by the presence of a T-cell receptor on the cell surface, they are called T cells. The several subsets of T cells each have a distinct function; the majority of human T cells, termed alpha beta T cells, rearrange their alpha and beta chains on the cell receptor and are part of the adaptive immune system. Specialized gamma delta T cells, have invariant T-cell receptors with limited diversity, that can present antigens to other T cells and are considered to be part of the innate immune system. Effector cells are the superset of all the various T cell types that respond to a stimulus, such as co-stimulation; this includes helper, killer and other T cell types. Memory cells are their opposite counterpart that are longer lived to target future infections as necessary. T helper cells assist other white blood cells in immunologic processes, including maturation of B cells into plasma cells and memory B cells, activation of cytotoxic T cells and macrophages.
These cells are known as CD4+ T cells because they express the CD4 glycoprotein on their surfaces. Helper T cells become activated when they are presented with peptide antigens by MHC class II molecules, which are expressed on the surface of antigen-presenting cells. Once activated, they divide and secrete small proteins called cytokines that regulate or assist in the active immune response; these cells can differentiate into one of several subtypes, including TH1, TH2, TH3, TH17, TH9, or TFH, which secrete different cytokines to facilitate different types of immune responses. Signalling from the APC directs T cells into particular subtypes. Cytotoxic T cells destroy virus-infected cells and tumor cells, are implicated in transplant rejection; these cells are known as CD8+ T cells since they express the CD8 glycoprotein at their surfaces. These cells recognize their targets by binding to antigen associated with MHC class I molecules, which are present on the surface of all nucleated cells. Through IL-10, other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state, which prevents autoimmune diseases.
Antigen-naïve T cells expand and differentiate into memory and effector T cells after they encounter their cognate antigen within the context of an MHC molecule on the surface of a professional antigen presenting cell. Appropriate co-stimulation must be present at the time of antigen encounter for this process to occur. Memory T cells were thought to belong to either the effector or central memory subtypes, each with their own distinguishing set of cell surface markers. Subsequently, numerous new populations of memory T cells were discovered including tissue-resident memory T cells, stem memory TSCM cells, virtual memory T cells; the single unifying theme for all memory T cell subtypes is that they are long-lived and can expand to large numbers of effector T cells upon re-exposure to their cognate antigen. By this mechanism they provide the immune system with "memory" against encountered pathogens. Memory T cells may be either CD4+ or CD8+ and express CD45RO. Memory T cell subtypes: Central memory T cells express CD45RO, C-C chemokine receptor type 7, L-selectin.
Central memory T cells have intermediate to high expression of CD44. This memory subpopulation is found in the lymph nodes and in the peripheral circulation.. Effector memory T cells lack expression of CCR7 and L-selectin, they have intermediate to high expression of CD44. These memory T cells lack lymph node-homing receptors and are thus found in the peripheral circulation and tissues. TEMRA stands for terminally differentiated effector memory cells re-expressing CD45RA, a marker found on naive T cells. Tissue resident memory T cells occupy tissues without recirculating. One cell surface marker, associated with TRM is the integrin αeβ7. Virtual memory T cells differ from the other memory subsets in that they do not originate following a strong clonal expansion event. Thus, although this population as a whole is abundant within the peripheral circulation, individual virtual memory T cell clones reside at low frequencies. One theory is. Although CD8 virtual memory T cells were the first to be described, it is now known that CD4 virtual memory cells exist.
Regulatory T cells are crucial for the maintenance of immunological tolerance. Their major role is to shut down T cell-mediated immunity toward the end of an immune reaction and to suppress autoreactive T cells that escaped the process of negative selection in the thymus. Suppressor T cells along with Helper T cells can collectively be called Regulatory T cells due to their regulatory functions. Two major classes of CD4 + Treg cells have been described -- FOXP3 − Treg cells. Regulatory T cells can develop either during normal development in the thymus, are known as thymic Treg cells, or can be induced peripherally and are called peripherally derived Treg cel
White blood cell
White blood cells are the cells of the immune system that are involved in protecting the body against both infectious disease and foreign invaders. All white blood cells are produced and derived from multipotent cells in the bone marrow known as hematopoietic stem cells. Leukocytes are found throughout the body, including lymphatic system. All white blood cells have nuclei, which distinguishes them from the other blood cells, the anucleated red blood cells and platelets. Types of white blood cells can be classified in standard ways. Two pairs of broadest categories classify them either by cell lineage; these broadest categories can be further divided into the five main types: neutrophils, basophils and monocytes. These types are distinguished by their physical and functional characteristics. Monocytes and neutrophils are phagocytic. Further subtypes can be classified; the number of leukocytes in the blood is an indicator of disease, thus the white blood cell count is an important subset of the complete blood count.
The normal white cell count is between 4 × 109/L and 1.1 × 1010/L. In the US, this is expressed as 4,000 to 11,000 white blood cells per microliter of blood. White blood cells make up 1% of the total blood volume in a healthy adult, making them less numerous than the red blood cells at 40% to 45%. However, this 1 % of the blood makes a large difference to health. An increase in the number of leukocytes over the upper limits is called leukocytosis, it is normal. It is abnormal, when it is neoplastic or autoimmune in origin. A decrease below the lower limit is called leukopenia; this indicates a weakened immune system. The name "white blood cell" derives from the physical appearance of a blood sample after centrifugation. White cells are found in the buffy coat, a thin white layer of nucleated cells between the sedimented red blood cells and the blood plasma; the scientific term leukocyte directly reflects its description. It is derived from the Greek roots leuk- meaning "white" and cyt- meaning "cell".
The buffy coat may sometimes be green if there are large amounts of neutrophils in the sample, due to the heme-containing enzyme myeloperoxidase that they produce. All white blood cells are nucleated, which distinguishes them from the anucleated red blood cells and platelets. Types of leukocytes can be classified in standard ways. Two pairs of broadest categories classify them either by cell lineage; these broadest categories can be further divided into the five main types: neutrophils, basophils and monocytes. These types are distinguished by their physical and functional characteristics. Monocytes and neutrophils are phagocytic. Further subtypes can be classified. Granulocytes are distinguished from agranulocytes by their nucleus shape and by their cytoplasm granules; the other dichotomy is by lineage: Myeloid cells are distinguished from lymphoid cells by hematopoietic lineage. Lymphocytes can be further classified as T cells, B cells, natural killer cells. Neutrophils are the most abundant white blood cell, constituting 60-70% of the circulating leukocytes, including two functionally unequal subpopulations: neutrophil-killers and neutrophil-cagers.
They defend against fungal infection. They are first responders to microbial infection, they are referred to as polymorphonuclear leukocytes, although, in the technical sense, PMN refers to all granulocytes. They have a multi-lobed nucleus; this gives the neutrophils the appearance of having multiple nuclei, hence the name polymorphonuclear leukocyte. The cytoplasm may look transparent because of fine granules. Neutrophils are active in phagocytosing bacteria and are present in large amount in the pus of wounds; these cells are not able to die after having phagocytosed a few pathogens. Neutrophils are the most common cell type seen in the early stages of acute inflammation; the life span of a circulating human neutrophil is about 5.4 days. Eosinophils compose about 2-4% of the WBC total; this count fluctuates throughout the day and during menstruation. It rises in response to allergies, parasitic infections, collagen diseases, disease of the spleen and central nervous system, they are rare in the blood, but numerous in the mucous membranes of the respiratory and lower urinary tracts.
They deal with parasitic infections. Eosinophils are the predominant inflammatory cells in allergic reactions; the most important causes of eosinophilia include allergies such as asthma, hay fever, hives. They secrete chemicals that destroy these large parasites, such as hook worms and tapeworms, that are too big for any one WBC to phagocytize. In general, their nucleus is bi-lobed; the lobes are connected by a thin strand. The cytoplasm is full of granules that assume a characteristic pink-orange color with eosin stain
International Standard Serial Number
An International Standard Serial Number is an eight-digit serial number used to uniquely identify a serial publication, such as a magazine. The ISSN is helpful in distinguishing between serials with the same title. ISSN are used in ordering, interlibrary loans, other practices in connection with serial literature; the ISSN system was first drafted as an International Organization for Standardization international standard in 1971 and published as ISO 3297 in 1975. ISO subcommittee TC 46/SC 9 is responsible for maintaining the standard; when a serial with the same content is published in more than one media type, a different ISSN is assigned to each media type. For example, many serials are published both in electronic media; the ISSN system refers to these types as electronic ISSN, respectively. Conversely, as defined in ISO 3297:2007, every serial in the ISSN system is assigned a linking ISSN the same as the ISSN assigned to the serial in its first published medium, which links together all ISSNs assigned to the serial in every medium.
The format of the ISSN is an eight digit code, divided by a hyphen into two four-digit numbers. As an integer number, it can be represented by the first seven digits; the last code digit, which may be 0-9 or an X, is a check digit. Formally, the general form of the ISSN code can be expressed as follows: NNNN-NNNC where N is in the set, a digit character, C is in; the ISSN of the journal Hearing Research, for example, is 0378-5955, where the final 5 is the check digit, C=5. To calculate the check digit, the following algorithm may be used: Calculate the sum of the first seven digits of the ISSN multiplied by its position in the number, counting from the right—that is, 8, 7, 6, 5, 4, 3, 2, respectively: 0 ⋅ 8 + 3 ⋅ 7 + 7 ⋅ 6 + 8 ⋅ 5 + 5 ⋅ 4 + 9 ⋅ 3 + 5 ⋅ 2 = 0 + 21 + 42 + 40 + 20 + 27 + 10 = 160 The modulus 11 of this sum is calculated. For calculations, an upper case X in the check digit position indicates a check digit of 10. To confirm the check digit, calculate the sum of all eight digits of the ISSN multiplied by its position in the number, counting from the right.
The modulus 11 of the sum must be 0. There is an online ISSN checker. ISSN codes are assigned by a network of ISSN National Centres located at national libraries and coordinated by the ISSN International Centre based in Paris; the International Centre is an intergovernmental organization created in 1974 through an agreement between UNESCO and the French government. The International Centre maintains a database of all ISSNs assigned worldwide, the ISDS Register otherwise known as the ISSN Register. At the end of 2016, the ISSN Register contained records for 1,943,572 items. ISSN and ISBN codes are similar in concept. An ISBN might be assigned for particular issues of a serial, in addition to the ISSN code for the serial as a whole. An ISSN, unlike the ISBN code, is an anonymous identifier associated with a serial title, containing no information as to the publisher or its location. For this reason a new ISSN is assigned to a serial each time it undergoes a major title change. Since the ISSN applies to an entire serial a new identifier, the Serial Item and Contribution Identifier, was built on top of it to allow references to specific volumes, articles, or other identifiable components.
Separate ISSNs are needed for serials in different media. Thus, the print and electronic media versions of a serial need separate ISSNs. A CD-ROM version and a web version of a serial require different ISSNs since two different media are involved. However, the same ISSN can be used for different file formats of the same online serial; this "media-oriented identification" of serials made sense in the 1970s. In the 1990s and onward, with personal computers, better screens, the Web, it makes sense to consider only content, independent of media; this "content-oriented identification" of serials was a repressed demand during a decade, but no ISSN update or initiative occurred. A natural extension for ISSN, the unique-identification of the articles in the serials, was the main demand application. An alternative serials' contents model arrived with the indecs Content Model and its application, the digital object identifier, as ISSN-independent initiative, consolidated in the 2000s. Only in 2007, ISSN-L was defined in the
B cells known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype. They function in the humoral immunity component of the adaptive immune system by secreting antibodies. Additionally, B cells present secrete cytokines. In mammals, B cells mature in the bone marrow, at the core of most bones. In birds, B cells mature in the bursa of Fabricius, a lymphoid organ.. B cells, unlike the other two classes of lymphocytes, T cells and natural killer cells, express B cell receptors on their cell membrane. BCRs allow the B cell to bind to a specific antigen, against which it will initiate an antibody response. B cells develop from hematopoietic stem cells. HSCs first differentiate into multipotent progenitor cells common lymphoid progenitor cells. From here, their development into B cells occurs in several stages, each marked by various gene expression patterns and immunoglobulin H chain and L chain gene loci arrangements, the latter due to B cells undergoing VJ recombination as they develop.
B cells undergo two types of selection while developing in the bone marrow to ensure proper development. Positive selection occurs through antigen-independent signaling involving both the pre-BCR and the BCR. If these receptors do not bind to their ligand, B cells do not receive the proper signals and cease to develop. Negative selection occurs through the binding of self-antigen with the BCR; this negative selection process leads to a state of central tolerance, in which the mature B cells don't bind with self antigens present in the bone marrow. To complete development, immature B cells migrate from the bone marrow into the spleen as transitional B cells, passing through two transitional stages: T1 and T2. Throughout their migration to the spleen and after spleen entry, they are considered T1 B cells. Within the spleen, T1 B cells transition to T2 B cells. T2 B cells differentiate into either follicular B cells or marginal zone B cells depending on signals received through the BCR and other receptors.
Once differentiated, they are now considered naive B cells. B cell activation occurs in the secondary lymphoid organs, such as the lymph nodes. After B cells mature in the bone marrow, they migrate through the blood to SLOs, which receive a constant supply of antigen through circulating lymph. At the SLO, B cell activation begins when the B cell binds to an antigen via its BCR. Although the events taking place after activation have yet to be determined, it is believed that B cells are activated in accordance with the kinetic segregation model determined in T lymphocytes; this model denotes that before antigen stimulation, receptors diffuse through the membrane coming into contact with Lck and CD45 in equal frequency, rendering a net equilibrium of phosphorylation and non-phosphorylation. It is only when the cell comes in contact with an antigen presenting cell that the larger CD45 is displaced due to the close distance between the two membranes; this allows for net phosphorylation of the BCR and the initiation of the signal transduction pathway.
Of the three B cell subsets, FO B cells preferentially undergo T cell-dependent activation while MZ B cells and B1 B cells preferentially undergo T cell-independent activation. B cell activation is enhanced through the activity of CD21, a surface receptor in complex with surface proteins CD19 and CD81; when a BCR binds an antigen tagged with a fragment of the C3 complement protein, CD21 binds the C3 fragment, co-ligates with the bound BCR, signals are transduced through CD19 and CD81 to lower the activation threshold of the cell. It has been shown that CD20 is directly required for BCR signalling in B cells, therapeutically used anti-CD20 antibodies such rituximab eliminate the B cells that have a high potential for activation of the BCR signalling pathway, it has been described that BCR signalling and B cell activation is inhibited by p53 stabilization during DNA damage response. Antigens that activate B cells with the help of T-cell are known as T cell-dependent antigens and include foreign proteins.
They are named as such because they are unable to induce a humoral response in organisms that lack T cells. B cell response to these antigens takes multiple days, though antibodies generated have a higher affinity and are more functionally versatile than those generated from T cell-independent activation. Once a BCR binds a TD antigen, the antigen is taken up into the B cell through receptor-mediated endocytosis and presented to T cells as peptide pieces in complex with MHC-II molecules on the cell membrane. T helper cells follicular T helper cells, that were activated with the same antigen recognize and bind these MHC-II-peptide complexes through their T cell receptor. Following TCR-MHC-II-peptide binding, T cells express the surface protein CD40L as well as cytokines such as IL-4 and IL-21. CD40L serves as a necessary co-stimulatory factor for B cell activation by binding the B cell surface receptor CD40, which promotes B cell proliferation, immunoglobulin class switching, somatic hypermutation as well as sustains T cell growth and differentiation.
T cell-derived cytokines bound
Nobel Prize in Physiology or Medicine
The Nobel Prize in Physiology or Medicine, administered by the Nobel Foundation, is awarded yearly for outstanding discoveries in the fields of life sciences and medicine. It is one of five Nobel Prizes established in his will in 1895 by Swedish chemist Alfred Nobel, the inventor of dynamite. Nobel was interested in experimental physiology and wanted to establish a prize for scientific progress through laboratory discoveries; the Nobel Prize is presented at an annual ceremony on 10 December, the anniversary of Nobel's death, along with a diploma and a certificate for the monetary award. The front side of the medal displays the same profile of Alfred Nobel depicted on the medals for Physics and Literature; the reverse side is unique to this medal. The most recent Nobel prize was announced by Karolinska Institute on 1 October 2018, has been awarded to American James P. Allison and Japanese Tasuku Honjo – for their discovery of cancer therapy by inhibition of negative immune regulation; as of 2015, 106 Nobel Prizes in Physiology or Medicine have been awarded to 12 women.
The first one was awarded in 1901 to the German physiologist Emil von Behring, for his work on serum therapy and the development of a vaccine against diphtheria. The first woman to receive the Nobel Prize in Physiology or Medicine, Gerty Cori, received it in 1947 for her role in elucidating the metabolism of glucose, important in many aspects of medicine, including treatment of diabetes; some awards have been controversial. This includes one to António Egas Moniz in 1949 for the prefrontal lobotomy, bestowed despite protests from the medical establishment. Other controversies resulted from disagreements over, included in the award; the 1952 prize to Selman Waksman was litigated in court, half the patent rights awarded to his co-discoverer Albert Schatz, not recognized by the prize. The 1962 prize awarded to James D. Watson, Francis Crick and Maurice Wilkins for their work on DNA structure and properties did not acknowledge the contributing work from others, such as Oswald Avery and Rosalind Franklin who had died by the time of the nomination.
Since the Nobel Prize rules forbid nominations of the deceased, longevity is an asset, considering prizes are awarded as long as 50 years after the discovery. Forbidden is awarding any one prize to more than three recipients. In the last half century there has been an increasing tendency for scientists to work as teams, resulting in controversial exclusions. Alfred Nobel was born on 21 October 1833 in Stockholm, into a family of engineers, he was a chemist and inventor who amassed a fortune during his lifetime, most of it from his 355 inventions of which dynamite is the most famous. He was interested in experimental physiology and set up his own labs in France and Italy to conduct experiments in blood transfusions. Keeping abreast of scientific findings, he was generous in his donations to Ivan Pavlov's laboratory in Russia, was optimistic about the progress resulting from scientific discoveries made in laboratories. In 1888, Nobel was surprised to read his own obituary, titled "The merchant of death is dead", in a French newspaper.
As it happened, it was Nobel's brother Ludvig who had died, but Nobel, unhappy with the content of the obituary and concerned that his legacy would reflect poorly on him, was inspired to change his will. In his last will, Nobel requested that his money be used to create a series of prizes for those who confer the "greatest benefit on mankind" in physics, peace, physiology or medicine, literature. Though Nobel wrote several wills during his lifetime, the last was written a little over a year before he died at the age of 63; because his will was contested, it was not approved by the Storting until 26 April 1897. After Nobel's death, the Nobel Foundation was set up to manage the assets of the bequest. In 1900, the Nobel Foundation's newly created statutes were promulgated by Swedish King Oscar II. According to Nobel's will, the Karolinska Institute in Sweden, a medical school and research center, is responsible for the Prize in Physiology or Medicine. Today, the prize is referred to as the Nobel Prize in Medicine.
It was important to Nobel that the prize be awarded for a "discovery" and that it be of "greatest benefit on mankind". Per the provisions of the will, only select persons are eligible to nominate individuals for the award; these include members of academies around the world, professors of medicine in Sweden, Norway and Finland, as well as professors of selected universities and research institutions in other countries. Past Nobel laureates may nominate; until 1977, all professors of Karolinska Institute together decided on the Nobel Prize in Physiology or Medicine. That year, changes in Swedish law forced the Institute to make public any documents pertaining to the Nobel Prize and it was considered necessary to establish a independent body for the Prize work. Therefore, the Nobel Assembly was constituted, it elects the Nobel Committee with 5 members who evaluate the nominees, the Secretary, in charge of the organization, each year 10 adjunct members to assist in the evaluation of candidates. In 1968, a provision was added.
True to its mandate, the Committee has chosen researchers working in the basic sciences over those who have made applied science contributions. Harvey Cushing, a pioneering American neurosurgeon who identified Cushing's syndrome, was not awarded the prize, nor was Sigmund Freud, as his psychoanalysis lacks hypotheses that can be experimentally confirmed; the public expected Jonas Salk or Albert Sabin to receive th
A micrograph or photomicrograph is a photograph or digital image taken through a microscope or similar device to show a magnified image of an object. This is opposed to a macrograph or photomacrograph, an image, taken on a microscope but is only magnified less than 10 times. Micrography is the art of using microscopes to make photographs. A micrograph contains extensive details of microstructure. A wealth of information can be obtained from a simple micrograph like behavior of the material under different conditions, the phases found in the system, failure analysis, grain size estimation, elemental analysis and so on. Micrographs are used in all fields of microscopy. A light micrograph or photomicrograph is a micrograph prepared using an optical microscope, a process referred to as photomicroscopy. At a basic level, photomicroscopy may be performed by connecting a camera to a microscope, thereby enabling the user to take photographs at reasonably high magnification. Scientific use began in England in 1850 by Prof Richard Hill Norris FRSE for his studies of blood cells.
Roman Vishniac was a pioneer in the field of photomicroscopy, specializing in the photography of living creatures in full motion. He made major developments in light-interruption photography and color photomicroscopy. Photomicrographs may be obtained using a USB microscope attached directly to a home computer or laptop. An electron micrograph is a micrograph prepared using an electron microscope. Micrographs have micron bars, or magnification ratios, or both. Magnification is a ratio between the size of an object on its real size. Magnification can be a misleading parameter as it depends on the final size of a printed picture and therefore varies with picture size. A scale bar, or micron bar, is a line of known length displayed on a picture; the bar can be used for measurements on a picture. When the picture is resized the bar is resized making it possible to recalculate the magnification. Ideally, all pictures destined for publication/presentation should be supplied with a scale bar. All but one of the micrographs presented on this page do not have a micron bar.
The microscope has been used for scientific discovery. It has been linked to the arts since its invention in the 17th century. Early adopters of the microscope, such as Robert Hooke and Antonie van Leeuwenhoek, were excellent illustrators. After the invention of photography in the 1820s the microscope was combined with the camera to take pictures instead of relying on an artistic rendering. Since the early 1970s individuals have been using the microscope as an artistic instrument. Websites and traveling art exhibits such as the Nikon Small World and Olympus Bioscapes have featured a range of images for the sole purpose of artistic enjoyment; some collaborative groups, such as the Paper Project have incorporated microscopic imagery into tactile art pieces as well as 3D immersive rooms and dance performances. Close-up Digital microscope Macro photography Microphotograph Microscopy USB microscope Make a Micrograph – This presentation by the research department of Children's Hospital Boston shows how researchers create a three-color micrograph.
Shots with a Microscope – a basic, comprehensive guide to photomicrography Scientific photomicrographs – free scientific quality photomicrographs by Doc. RNDr. Josef Reischig, CSc. Micrographs of 18 natural fibres by the International Year of Natural Fibres 2009 Seeing Beyond the Human Eye Video produced by Off Book - Solomon C. Fuller bio Charles Krebs Microscopic Images Dennis Kunkel Microscopy Andrew Paul Leonard, APL Microscopic Cell Centered Database - Montage Nikon Small World Olympus Bioscapes Other examples