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Koch himself became aware of the limitations of his postulates upon discovery that Vibrio cholerae treatment xdr tb guidelines 2mg leukeran buy fast delivery, the agent of cholera, could be isolated from both sick and healthy individuals. For example, the first postulate, which states that the microorganism must be "regularly associated" with the disease, does not hold true for many animal reservoirs, such as bats, in which the virus actively reproduces but causes no disease. Similarly, arthropod vectors, such as mosquitoes, support reproduction of a variety of hemorrhagic viruses but do not themselves die of such infections. However, many viruses, including papillomaviruses that cause warts and cervical cancer and hepatitis B virus that causes liver cirrhosis and cancer, cannot be cultured, or require complex culture conditions that must mimic the tissue complexity found in the infected host. Consequently, it is generally accepted that the postulates are a guide, not an invariant set of requirements to fulfill. Such approaches alleviate the requirement to culture the suspected agent and are sufficiently sensitive to detect the presence of vanishingly small quantities of viral nucleic acid in an apparently healthy individual. Assiduously applying the postulates has been particularly problematic for identifying viruses that cause human tumors. This commission was formed in part because of the high incidence of the disease among soldiers who were occupying Cuba. In retrospect, a mosquito-borne mode of transmission made sense, as the disease was predominately found in warm and humid regions of the world. The nature of the pathogen was established in 1901, when Reed and James Carroll injected diluted, filtered serum from the blood of a yellow fever patient into three healthy individuals. Two of the volunteers developed yellow fever, causing Reed and Carroll to conclude that a "filterable agent," which we now know as yellow fever virus, was the cause of the disease. In the same year, Juan Guiteras, a professor of pathology and tropical medicine at the University of Havana, attempted to produce immunity by exposing volunteers to mosquitoes that were allowed to take a blood meal from an individual who showed signs of yellow fever. Her agreement to be infected a second time was to test if her earlier exposure provided protection from a subsequent challenge. This was a prescient idea, because at that time, virtually nothing was known about immune memory. Yellow fever had been endemic in Havana for 150 years, but the conclusions of Reed and his colleagues about the nature of the pathogen and the vector that transmitted it led to rapid implementation of effective mosquito control measures that dramatically reduced the incidence of disease within a year. To this day, mosquito control remains an important method for preventing yellow fever, as well as other viral diseases transmitted by arthropod vectors. However, the pace of discovery was slow, in great part because of the dangers and difficulties associated with experimental manipulation of human viruses so vividly illustrated by the experience with yellow fever virus. Consequently, agents of some important human diseases were not identified for many years and only then with some good luck. A classic example is the identification of the virus responsible for influenza, a name derived in the mid-1700s from the Italian language because of the belief that the disease resulted from the "influence" of contaminated air and adverse astrological signs. Worldwide epidemics (pandemics) of influenza had been documented in humans for well over 100 years. Such pandemics were typically associated with mortality among the very young and the very old, but the 1918-1919 pandemic following the end of World War I was especially devastating. Despite many efforts, a human influenza virus was not isolated until 1933, when Wilson Smith, Christopher Andrewes, and Patrick Laidlaw serendipitously found that the virus could be propagated in an unusual host.
Tools of Epidemiology We have considered some of the terms that epidemiologists use medicine while pregnant discount 5 mg leukeran with amex, but how do these scientists monitor and develop strategies to control the spread of viruses in populations An investigation begins at the site of an outbreak, where as much descriptive data as possible about the infected cases and the environment are gathered. In cases of viral infections in humans, information on recent travel, lifestyle, and preexisting health conditions is considered, along with the medical records of infected individuals to generate a testable hypothesis about the origin of the outbreak. The word "descriptive" can have a negative connotation in virology and is often used to mean the opposite of "mechanistic. Following the descriptive phase, analytical epidemiological methods are used to test hypotheses using control populations in either retrospectively or prospectively focused studies. Clinical epidemiology focuses on the collection of biospecimens, such as blood, sputum, urine, and feces, to search for viral agents or other pathogens and to help determine the potential route of transmission. Once specimens are collected, nucleic acid sequencing is often performed on the samples. In addition, such studies may include serological analyses, in which antibodies in the blood that implicate previous infection are identified. Often the effects are subtle, or the data are highly varied from sample to sample or from study to study (sometimes referred to as "noise"). This ambiguity is particularly true in epidemiological studies, given the large number of parameters and potential outcomes. How do you know if the data that you generated (or that you are reading about in a paper) are significant Statistical methods, properly employed, provide the common language of critical analysis to determine whether differences observed between or among groups are significant (Table 1. Unfortunately, surveys of articles published in scientific journals indicate that statistical errors are common, making it even more difficult for the reader to interpret results. In fact, the term "significant difference" may be one of the most misused phrases in scientific papers, because the actual statistical support for the statement is often absent or incorrectly derived. While a detailed presentation of basic statistical considerations for virology experiments is beyond the scope of this text, some guiding principles are offered. It is essential to consider experimental design carefully before going to the bench or to the field. A fundamental challenge in study design is to predict correctly the number of observations required to detect a significant difference. The significance level is defined as the probability of mistakenly saying that a difference is meaningful; typically, this probability is set at 0. Scientists do not usually refer to things as "true" or "false" but rather use quantitative approaches to provide a sense of the significance between two data sets. An important concept is power, the probability of detecting a difference that truly is significant. In the simplest case, power can be increased by having a larger sample size (Table 1.
Diseases
Malnutrition increases susceptibility to infection because the physical barriers treatment laryngitis buy generic leukeran 2mg on-line, as well as immune fitness, are compromised. An example is the increased susceptibility to measles in children with protein deficiency. Such severe measles infections are observed in children in tropical Africa and in aboriginal children in Australia. As virologists begin to view individuals as products of their histories, genetics, environments, and life choices, rather than as masses of permissive cells and tissues, a more complete picture of susceptibility to an infection will emerge. These hormones have an anti-inflammatory effect, which is thought to limit tissue damage. Similarly, cigarette smoking increases susceptibility to respiratory infections as a result of the decreased capacity of the tar-coated lungs and airways to self-clean. We often refer to "our defenses being down," but what this probably means is that the balance of hormones that maintain homeostasis is altered, creating opportunities for a viral infection. Perspectives A fundamental principle of virology is that for a virus to be maintained in a host population, virus particles must be released from one infected host to infect another. This process of serial infection, while simple in principle, is difficult to study in natural systems given the mind-boggling number of host, viral, and environmental variables. Nevertheless, epidemiology, the study of this process, is evolving rapidly as new ways to track and identify infectious agents are developed. To thwart a potential epidemic, viral epidemiologists must possess the skills of a private investigator, sociologist, conductor, and chef at a popular restaurant. To track the origins of infection, epidemiologists must consider simultaneously multiple variables and clues, some of which are false leads. These investigators must understand the dynamics of the animal or human populations at risk and how aspects of behavior might increase the potential for infection. They must then integrate these diverse pieces of information, and because the investigation often begins only once an epidemic is under way and victims have been identified, epidemiologists must be able to work under great pressure, within a constrained time frame, and often under intense media scrutiny. At the writing of this text, an Ebola outbreak in Africa has begun, killing thousands of people. Doctors cannot document all of the new cases, and many individuals who are ill are staying in their homes, fearful of the government response. Many believe that going to a clinic for care will isolate them from their families. Containing an epidemic under such pressures is a monumental challenge, especially when no certain therapy exists that can be offered to patients. The goal of epidemiology in this setting is to define the basis of the outbreak and to limit further transmission. Fortunately, Ebola virus is only transmitted via bodily fluids, such as blood and sputum; if this highly lethal virus could be acquired by means of aerosol droplets, the epidemiological challenge would obviously be far greater. Our current understanding of the fundamental principles of viral pathogenesis comes largely from studies with animal models. For example, use of the large number of genetically identical, available mouse strains has led to the identification of many genes that confer susceptibility to particular viral infections.
Although serious side effects are uncommon treatment of schizophrenia purchase 2 mg leukeran otc, pulmonary toxicity is the most feared and can present either with an acute onset after a short course of therapy or with a chronic insidious onset after months or years of therapy. Clinical manifestations include a variety of nonspecific respiratory symptoms, such as dyspnea, dry cough, and fatigue. Laboratory findings are also nonspecific but often include peripheral eosinophilia or leukocytosis. As with most adverse drug reactions, the diagnosis of nitrofurantoin-induced pneumonitis requires a high index of clinical suspicion, in combination with careful clinicopathologic correlation. Although a presumptive clinical diagnosis is sufficient in most cases, lung biopsies may be performed in patients with more severe disease or in whom there is higher concern for infection or malignancy. Other patterns of acute lung injury, including diffuse alveolar damage or organizing pneumonia. Less commonly, granulomatous interstitial pneumonia or 1239 features of giant-cell interstitial pneumonia can be seen. Differential Diagnosis As nitrofurantoin-induced pulmonary toxicity is associated with diverse histologic findings but no specific features, a variety of other conditions may enter the differential diagnosis, depending on the specific injury pattern(s) encountered in an individual case. Acute infections should be excluded if there is evidence of acute or subacute injury (such as diffuse alveolar damage or organizing pneumonia), and a careful evaluation for specific evidence of infection should be performed, including a search for viral inclusions and special stains for microorganisms as appropriate. A systemic connective tissue disease is another common consideration with most of these reaction patterns. Unfortunately, there are no specific histologic features to distinguish between these two possibilities, and correlation with clinical and serologic findings is essential. Hypersensitivity pneumonitis may be a consideration, if cellular interstitial pneumonia and/or granulomas are seen, and this diagnosis also requires clinicopathologic correlation. When significant fibrosis is present, other forms of chronic fibrosing interstitial pneumonia may also enter the differential diagnosis, and multidisciplinary discussion is usually required to establish the correct diagnosis. This pattern is nonspecific and may also be seen with chronic infections (particularly atypical mycobacterial infection), aspiration, hot tub lung, hypersensitivity pneumonitis, connective tissue diseases, and other drug reactions. These drugs target serotonergic signaling pathways to increase the bioavailability of serotonin, thereby producing appetite suppression via effects on relevant neural networks in the central nervous system. Unfortunately, elevated serotonin also induces proliferation of arterial smooth muscle cells, adventitial fibroblasts, and epithelial cells in the lung, leading to pulmonary arterial hypertension in some patients. Fibroproliferative intimal lesions are typically present in arteries of all sizes, including large elastic conduit arteries, medium-sized muscular arteries, and small arteries.
Susceptible individuals are targets for infection and can develop disease and spread the virus to others medicine quotes leukeran 5 mg purchase on line. The persistence of a virus in a population depends on the presence of a sufficient number of those who are vulnerable. Immunization against viral infection by natural infection or vaccination reduces the number of potential hosts and therefore limits the foothold that a virus can establish in a community. For example, epidemics of polio were self-limiting, because the asymptomatic spread of the virus immunized the population. The competence of the immune response also determines the speed and efficiency with which an infection is spread and resolved and the severity of symptoms. This hypothesis is supported by the observations that individuals from isolated populations. For example, intracerebral inoculation of lymphocytic choriomeningitis virus in adult mice is lethal because recruitment of T cells into the brain leads to swelling and death. In contrast, infant mice survive this challenge because of their weaker response (Box 1. Some viral infections, including those caused by poliovirus, mumps virus, and measles virus, are less severe in children than in adults, perhaps because the robust adult response contributes to disease. It has been suggested that the increased death rate in young adults was caused by an overly aggressive immune response that flooded their systems with cytokines, sometimes referred to as a "cytokine storm. Unfortunately, many animal models of congenital brain infections do not mimic human disease for a variety of poorly understood reasons. In contrast, the neonatal rat model for congenital lymphocytic choriomeningitis virus infection reproduces virtually all the neuropathological changes observed in congenitally infected humans. Within the developing rat brain, the virus selectively infects mitotically active neuronal precursors, a fact that explains the variation in pathology with time of infection during gestation. Lymphocytic choriomeningitis virus infection results in delayed-onset neuronal loss after the virus has been cleared by the immune system. Accordingly, many researchers think that this model can be used to study neurodegenerative or psychiatric diseases associated with loss of neurons or their function. Congenital viral infection of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat. Nongenetic Risk Factors Nongenetic risk factors include age, health, lifestyle, and occupation. In a classic story of virology history, Edward Jenner noticed that milkmaids appeared immune to smallpox, a trait that was later found to be due to "vaccination" by a relative of smallpox that infected cows. The age of the host also plays an important role in determining the result of viral infections.
An attendant benefit from such a mechanism would be the selection for genomes that express functional P protein medications major depression discount leukeran 2 mg buy line. Hepadnaviral reverse transcription is distinguished by the fact that the primer and the polymerase are within a single protein. The highly conserved residues in the homologous domains are essential for hepadnaviral reverse transcription. If is not present during synthesis of P protein in yeast, the enzyme is inactive, even if is supplied later. Consequently, binding to may be required for the P protein to fold into an active conformation. Furthermore, incorporation of these host cell proteins into viral capsids appears to require the polymerase activity of P protein. Critical Steps in Reverse Transcription Initiation and the first template exchange. This single protein molecule acts both as primer and catalyst for all subsequent steps in reverse transcription (Box 7. P protein remains covalently attached to the 5 end of the strand during the first template exchange and, as noted previously, through all subsequent steps. Nevertheless, it is widely believed among hepadnavirus researchers that there is only one P molecule in an infectious particle. Furthermore, even though the two functional domains are separated by a hinge, a P variant with a mutation in the terminal protein cannot complement a variant with a mutation in the polymerase domain. It seems likely that hepadnaviral core architecture and components help to ensure that the required interactions between P protein and nucleic acid templates can occur in such a way that exchanges are facilitated and templates can transit to the active site as product strands are synthesized. In a cross section, the outer portion of the core is assembled from C protein dimers (gray). Additional internal (blue) density represents unidentified encapsidated proteins and/or misaligned capsid. As in the first template exchange, a particular organization of the template in the core particles is thought to facilitate the process. The first template exchange (step 2) is promoted by interaction with a sequence that lies between dr1 and dr2 at the 3 end of the pregenome. Mutation of the normal acceptor sequence leads to the synthesis of strands with 5 ends that map to other sites in the vicinity of the 3 dr1, which apparently can serve as alternative acceptors. A deletion analysis with the woodchuck virus has suggested that a region 1 kb upstream of the 3 dr1 includes a signal that specifies the acceptor site. At a low frequency (5 to 10%), the strand primer is extended in situ instead of being translocated (the structure set off by a dashed arrow) (step 5a); elongation of this strand results in a duplex linear genome.
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Note the clear separation of the profiles from uninfected persons and infected patients symptoms you have worms purchase leukeran 5mg amex, and the dispersal of those from elite controllers in both clusters. Differences between the infected and mock-infected samples identified by microarray hybridization are shown for cytokine response, lipid metabolism, and coagulation genes. The latter changes were also observed in animals infected by the highly pathogenic 1918 H1N1 influenza virus, although their significance is not yet known. It has been suggested that such a gene expression signature of highly pathogenic influenza viruses could help identify new therapeutics that target specific host proteins or pathways. H7N9 and other pathogenic avian influenza viruses elicit a three-pronged transcriptomic signature that is reminiscent of 1918 influenza virus and is associated with a lethal outcome in mice. Metabolism Host cells supply not only the molecular machinery needed for synthesis of viral nucleic acids and proteins (at a minimum the translational machinery), but also the essential building blocks, nucleotides and amino acids. Assembly of enveloped viruses also requires cellular membranes and the lipids from which these structures are constructed. Consequently, virus infection can lead to alterations in the pathways by which cells generate energy from molecular fuels (catabolism), as well as those that make the precursors of nucleic acids, proteins, and membranes (anabolism). Perhaps not surprisingly, the impact of infection on host metabolism is virus specific, ranging from relatively simple alterations in the rates of particular reactions to extensive redirection of multiple pathways to virus-specific ends. Indeed, infection by some viruses has been associated with development of metabolic diseases. It has therefore been appreciated for decades that virus infection modulates cellular energy metabolism, often increasing the rate of glycolysis. However, this aspect of virus-host cell interactions was difficult to study in detail until the development of methods for simultaneous and comprehensive measurement of the concentrations of large numbers of metabolites and of changes in flux through individual pathways and reactions, so-called metabolomics. In the past decade or so, application of these methods to virus-infected cells (and their mock-infected counterparts) has revealed just how extensive the modulation of catabolism or anabolism can be, and unexpected ways in which virus infection can redirect metabolic networks. Substrates and intermediates of metabolic pathways turn over as they are converted to other compounds, and many do so at high rates. Accurate measurement of the concentrations of metabolites under a particular condition therefore requires that metabolic pathways be halted quickly as samples are collected. This imperative is typically met by rapidly transferring cells to ice-cold organic solvents, a process that also contributes to extraction of metabolites. These compounds are then separated and identified by a variety of analytic techniques, most commonly liquid or gas chromatography followed by one- or two-dimensional mass spectrometry. The ions separated in this way are identified by comparison of their properties to the contents of reference libraries of metabolites, and can be quantified.
This unusual property is thought to help retroviruses survive extensive damage to their genomes (Chapter 7) medicine and technology order 2 mg leukeran. It has therefore been suggested that one function of this protein is to stabilize the protein shell so that it can withstand the pressure exerted by the encapsidated genome. Sequences necessary for packaging of retroviral genomes, termed psi, vary considerably in complexity and location. These models were confirmed by various observations, including the results of site-directed mutagenesis. Specific signals may be required to mark a viral genome for encapsidation, but their presence does not guarantee packaging. The fixed dimensions of the closed icosahedral capsids or nucleocapsids of many viruses impose an upper limit on the size of viral nucleic acid that can be accommodated. Consequently, even when they contain appropriate packaging signals, nucleic acids that are more than 5 to 10% larger than the wild-type genome cannot be encapsidated. The specificity with which the viral genome is incorporated into assembling structures may also be the result of the coupling of encapsidation with its synthesis. It was deduced from these properties that the T4 genome is circularly permuted and terminally redundant. Furthermore, when sequences are deleted from, or inserted into, the genome, the length of the terminal repeats increases or decreases to the corresponding degree. Initial cleavage between H and A is followed by packaging of a headful length that is longer than the length of the unique genome sequence, and the second cleavage. It has been appreciated for many years that formation of an infectious virus particle requires incorporation of at least one copy of each of the eight genomic segments. Packaging of the bacteriophage 6 genome provides clear precedent for a selective mechanism. This ratio might seem impossibly low, but it is within the range of ratios of noninfectious to infectious particles found in virus preparations. Nevertheless, it has become clear in the last decade that the packaging of influenza virus genome segments is selective. These sequences comprise the short 5 and 3 noncoding regions of each segment but extend short distances into adjacent coding regions. Purified influenza A virus particles were examined by scanning transmission electron tomography. In most cases, the precursors to these enzymes are synthesized as C-terminal extensions of the Gag polyprotein. The low efficiency with which Gag-Pol polyproteins are translated determines their concentrations relative to Gag in the cell and in virus particles (1:9).
Peribronchiolitis with lymphoid hyperplasia world medicine buy leukeran 5 mg with mastercard, often as nodular aggregates of lymphocytes. Because of the rarity of the disease, treatment strategies are not well characterized. Treatment most often includes corticosteroids, 935 and removal from further flock exposure is probably the best measure to prevent progression of disease. Differential Diagnosis the differential diagnosis for the characteristic histologic changes in flock lung is broad. IgG4-related pulmonary disease usually has a component of fibrosis, which is more extensive than what is seen in flock lung. In addition, immunohistochemistry for IgG4 and IgG can help exclude this possibility. Note the peribronchiolar chronic inflammatory cell infiltrate consisting mostly of lymphocytes. Smith Raghavendra Pillappa Over the past 15 years, there has been increased recognition of a potential idiopathic interstitial lung disease that is centered around airways and shows variable fibroinflammatory changes. Because of this increased recognition, the 2013 update on idiopathic interstitial pneumonias from the American Thoracic Society and European Respiratory Society included the term bronchiolocentric patterns of interstitial pneumonia under the section of rare histologic patterns. Airway-centered fibrosis is one of the main patterns of injury seen in his setting. Additional study will be required to determine if this represents a true idiopathic interstitial pneumonia or is secondary to another form of chronic centrilobular injury, perhaps inhalational. Patients with airway-centered fibrosis typically present with chronic cough and slowly progressive dyspnea. Patients showed a predominantly restrictive pattern with decreased forced vital capacity on pulmonary function testing. Imaging studies often show centrilobular changes with traction bronchiectasis, interstitial thickening, and fibrosis. Histologic Features At scanning magnification, one can appreciate "stellate" appearing scars beginning in the centrilobular regions. There is often extensive chronic small airways remodeling in the background including peribronchiolar metaplasia with extension of respiratory epithelium into adjacent alveoli (bronchiolization) and mucostasis. The presence of foreign material is suggestive of aspiration predominantly chronic aspiration of gastric contents. The presence of scattered interstitial granulomas and multinucleated giant cells is suggestive of chronic hypersensitivity pneumonitis. Because of insufficient studies of these patients and lack of adequate clinical follow-up, it has been difficult to suggest a treatment strategy. Airway-centered fibrosis must be distinguished from fibrotic nonspecific interstitial pneumonia and from the usual interstitial pneumonia pattern of pulmonary fibrosis. This is best done at low centered fibrosis, which are in contrast to the peripheral and subpleural predominant scars as seen in the usual interstitial pneumonia pattern of fibrosis.
Disease can be especially severe in premature infants and in the immunocompromised individuals medicinenetcom leukeran 5mg with visa. Histologic Features Conducting airways show evidence of epithelial injury and regeneration, with basal layer hyperplasia that can eventually result in squamous metaplasia. This infection causes progressive pulmonary edema and acute respiratory distress syndrome and can occur in otherwise healthy individuals. Histologic Features A mild mononuclear interstitial inflammation is seen along with edema. This progresses to diffuse alveolar damage with hyaline membranes and type 2 pneumocyte hyperplasia. Pneumococcal pneumonia can be complicated by bacteremia, pericarditis, and empyema. Although young children and elderly individuals are more susceptible to pneumonia and prone to complications, pneumococcal pneumonia remains a significant cause of pneumonia in otherwise healthy adults. Pneumococcal vaccine can prevent infection and is offered to patients older than 65 years, as well as to those with immunocompromised states, hemoglobinopathies, and asplenia. Acute infection consists of intra-alveolar accumulation of neutrophils; with time, organization includes an influx of macrophages. This can occur via aspiration, via mechanical ventilation, and in situations where normal airway function is compromised (such as postviral airway metaplasia). In addition, Staphylococcus can reach the lung via the bloodstream, for example, in patients with bacterial 1056 endocarditis. The tendency of this organism to cause necrotizing pneumonia leads to abscess formation and can result in pleural extensions, resulting in empyema. Histologic Features Staphylococcal pneumonia is necrotizing and can result in abscess formation. The organism is a gram-positive coccus, and abundant organisms can be seen in sheets and clusters. In addition, it continues to be a wider health problem, as it has increased as a cause of hospital-acquired pneumonia. It is spread through contact and can affect individuals on ventilators and with intravenous catheters. Histologic Features As in other acute pneumonias, stages go from neutrophil influx to increasing numbers of macrophages, with resolution, organization, or scarring. However, patients with cystic fibrosis are susceptible to infection with Pseudomonas, as well as with Burkholderia cepacia and Stenotrophomonas maltophilia (formerly Pseudomonas cepacia and Pseudomonas maltophilia).
Bufford, 29 years: Once the sequences to which the chaperone binds are buried in the interior of the protein, such interactions cease. Histologic Features Lymphoepithelioma-like carcinoma is characterized by a syncytial arrangement of tumor cells with an infiltrate of lymphocytes. Benign clear cell tumor of the lung ("sugar tumor"): morphologic, immunohistochemical, and ultrastructural evaluation.
Jaroll, 56 years: Histologic Features 564 Well-circumscribed tumor with multiple cystic spaces filled with granular debris and lined by plump pneumocytes. When more than a few airspaces are involved, a careful search for neoplastic epithelium is in order because mucinous infiltrates may be a manifestation of mucinous bronchioloalveolar carcinoma. While reactivation from a single neuron is likely all or none, the virus is reactivated in only a small number of neurons within an infected ganglia.
Mitch, 60 years: Airway injury may be present characterized by necrosis of the epithelium or later by regenerative or metaplastic features. The viral and cellular members of this family are similar in sequence, particularly around the active site, and are also similar in three-dimensional structure. The cells may be confined to the mucosa, protrude into the lumen of the airway, or invade across the basal lamina forming tumorlets.
Anog, 39 years: Antigenic phenotype of malignant mesotheliomas and pulmonary adenocarcinomas: an immunohistologic analysis demonstrating the value of Leu-M1 antigen. It is commonly seen in middle-aged to older adults and is often preceded by a flu-like illness. Viral Scaffolding Proteins: Chaperones for Assembly Accurate assembly of some large icosahedral protein shells, such as those of adenoviruses and herpesviruses, is mediated by proteins that are not components of mature virus particles (Table 13.
Jesper, 49 years: Diverse Receptors Impart Antigen Specificity to B and T Cells Like the innate response, the adaptive response must distinguish infected from uninfected cells. It is a common misconception that discolored mucus is directly due to bacterial or viral presence, but the yellow or green mucus hue observed during infection is not due to bacteria or virus particles. Infection is most commonly bacterial, but fungal or nontuberculous mycobacterial infection may also occur.
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