Condet

Ricardo Roda, M.D., Ph.D.

• Assistant Professor of Neurology

https://www.hopkinsmedicine.org/profiles/results/directory/profile/10000730/ricardo-roda

A critical review of the clinical effects of therapeutic irradiation damage to the brain: the roots of controversy anxiety symptoms lingering discount 25 mg phenergan with amex. The cognitive effects of cranial irradiation are critically reviewed comparing risk factors such as age anxiety symptoms sweating buy phenergan 25 mg on-line, volume of brain irradiated anxiety symptoms pictures purchase 25 mg phenergan with amex, premorbid conditions anxiety symptoms without anxiety discount phenergan 25 mg free shipping, region of brain irradiated and dose. The authors offer observations and hypotheses which they suggest could be informative in the treatment decision process. Indicators of hippocampal neurogenesis are altered by 56Fe-particle irradiation in a dose-dependent manner. Radiation-induced cognitive impairments are associated with changes in indicators of hippocampal neurogenesis. Two-month-old mice received hippocampus/cortex irradiation (10 Gy) and were behaviorally tested 3 months later. Irradiated mice showed hippocampal-dependent spatial learning and memory impairments. These impairments were associated with decreased proliferation of cells and immature neurons on the subgranular zone of the dentate gyrus. The authors conclude that reduction in neurogenesis plays a contributory role in the pathogenesis of radiation-induced cognitive impairments. This article critically reviews the functional significance of neurogenesis in the adult. They conclude that there is sufficient evidence that such new neurons can function and suggest that they contribute to cognition. Age-dependent expression of glucocorticoid- and mineralocorticoid receptors on neural precursor cell populations in the adult murine hippocampus. The authors report that the strong negative regulatory effect which corticosteroids have on adult hippocampus may be mediated by both glucorticoid and mineralocorticoid receptors. Outcomes at school age after postnatal dexamethasone therapy for lung disease of prematurity. Authors conclude that the use of early postnatal dexamethasone therapy leads to substantial adverse effects on neuromotor and cognitive function at school age. This article adds to the growing literature on the adverse effects of corticosteroids on neurological function which may be mediated, in part, by reduction in neurogenesis. Suppression of hippocampal neurogenesis is associated with developmental stage, number of perinatal seizure episodes, and glucocorticosteroid level. Gene expression analysis in the hippocampal formation of tree shrews chronically treated with cortisol. Identification of genes regulated by chronic psychosocial stress and antidepressant treatment in the hippocampus. The cognitive sequelae of standard-dose adjuvant chemotherapy in women with breast carcinoma: results of a prospective, randomized, longitudinal trial. Longitudinal report of an association of cognitive impairment and chemotherapy in a group of women treated for nonmetastatic breast cancer. About half of the affected patients improved at the long-term post-chemotherapy time point. Neurocognitive performance in breast cancer survivors exposed to adjuvant chemotherapy and tamoxifen. The nature and severity of cognitive impairment associated with adjuvant chemotherapy in women with breast cancer: A meta-analysis of the current literature. Despite their relatively young age, they were found to have significant cognitive impairment and only 42% resumed work. Cognitive dysfunction in patients with pituitary tumour who have been treated with transfrontal or transsphenoidal surgery or medication. Cognitive effects of pituitary tumours and their treatments: two case studies and an investigation of 90 patients. Evaluation of the effect of radiotherapy for pituitary tumours on cognitive function and quality of life. Cognitive impairments were found to occur in patients undergoing radiotherapy for pituitary tumors; 27% of patients who underwent surgery and radiotherapy performed below the 10th percentile in three or more cognitive tests compared with 5% of patients undergoing surgery alone. Neuropsychological function in adults after high dose fractionated radiation therapy of skull base tumors.

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These proteins act in one of two ways: either they bind directly to a cytokine receptor but fail to activate the cell anxiety 7 scoring interpretation order 25mg phenergan free shipping, or they bind directly to a cytokine anxiety symptoms in males purchase phenergan 25 mg line, inhibiting its activity anxiety nightmares buy 25mg phenergan mastercard. It has been cloned and is currently being investigated as a potential treatment for chronic inflammatory diseases anxiety symptoms in spanish discount 25 mg phenergan. These soluble antagonists arise from enzymatic cleavage of the extracellular domain of cytokine receptors. For example, the neutralization of a soluble bacterial toxin requires antibodies, whereas the response to an intracellular virus or to a bacterial cell requires cell-mediated cytotoxicity or delayed-type hypersensitivity. This subset is also associated with the promotion of excessive inflammation and tissue injury. The antibody bound to the worm binds to the Fc receptors of eosinophils, thus forming an antigen-specific bridge between the worm and the eosinophils. The attack of the eosinophil on the worm is triggered by crosslinking of the Fc -bound IgE. They suggested instead that these subsets might represent different maturational stages of a single lineage. Key cytokines produced by each subset positively regulate the subset that produces it and negatively regulate the other subset. The critical role played by each of these cytokines and their receptors has been demonstrated in a series of experiments in which either the cytokine or its receptor has been knocked out. First, they promote the growth of the subset that produces them; second, they inhibit the development and activity of the opposite subset, an effect known as cross-regulation, (see Figure 12-12). The phenomenon of cross-regulation explains the observation that there is often an inverse relationship between antibody production and cell-mediated immunity; that is, when antibody production is high, cellmediated immunity is low, and vice versa. Recent work has given insight into the molecular basis for the cytokine-mediated cross-regulation by which one subset promotes its own expansion and development while inhibiting the development of the opposite subset. Consequently, cytokine signals that induce one of these transcription factors set in motion a chain of events that repress the other. In humans, a well-studied example of this phenomenon is leprosy, which is caused by Mycobacterium leprae, an intracellular pathogen that can survive within the phagosomes of macrophages. Leprosy is not a single clinical entity; rather, the disease presents as a spectrum of clinical responses, with two major forms of disease, tuberculoid and lepromatous, at each end of the spectrum. In tuberculoid leprosy, a cell-mediated immune response forms granulomas, resulting in the destruction of most of the mycobacteria, so that only a few organisms remain in the tissues. Although skin and peripheral nerves are damaged, tuberculoid leprosy progresses slowly and patients usually survive. In lepromatous leprosy, the cell-mediated response is depressed and, instead, humoral antibodies are formed, sometimes resulting in hypergammaglobulinemia. The mycobacteria are widely disseminated in macrophages, often reaching numbers as high as 1010 per gram of tissue. Lepromatous leprosy progresses into disseminated infection of the bone and cartilage with extensive nerve damage. This cytokine profile explains the diminished cell-mediated immunity and increased production of serum antibody in lepromatous leprosy. Cytokine-Related Diseases Defects in the complex regulatory networks governing the expression of cytokines and cytokine receptors have been implicated in a number of diseases. This section describes several diseases resulting from overexpression or underexpression of cytokines or cytokine receptors. Bacterial Septic Shock Is Common and Potentially Lethal the role of cytokine overproduction in pathogenesis can be illustrated by bacterial septic shock. This condition may develop a few hours after infection by certain gram-negative bacteria, including E. The symptoms of bacterial septic shock, which is often fatal, include a drop in blood pressure, fever, diarrhea, and widespread blood clotting in various organs. This condition afflicts about 500,000 Americans annually and causes more than 70,000 deaths. The annual cost for treating bacterial septic shock is estimated to be in excess of $5 billion. It is hoped that these experimental results will lead to clinically useful products for the treatment of bacterial septic shock in humans. Although these plasma cells are not malignant, the high rate of plasma-cell proliferation possibly contributes to the development of cancer.

The cumulative effect of multiple low doses of less than 10 mGy delivered over extended periods has to be explored further anxiety symptoms head pressure discount 25mg phenergan. The development of in vitro transformation assays utilizing nontransformed human diploid cells is judged to be of special importance anxiety symptoms like ms purchase phenergan 25 mg amex. Although less well established anxiety symptoms legs discount phenergan 25mg without prescription, the data available point toward a single-cell (monoclonal) origin for induced tumors and suggest that low-dose radiation acts predominantly as a tumor-initiating agent anxiety symptoms peeing order 25mg phenergan fast delivery. These data also provide some evidence on candidate, radiation-associated mutations in tumors. However, telomereassociated mechanisms did provide a coherent explanation for some in vitro manifestations of induced genomic instability. The data considered did not reveal consistent evidence for the involvement of induced genomic instability in radiation tumorigenesis, although telomere-associated processes may account for some tumorigenic phenotypes. Since, however, the induction or development of these two cancer types is believed to proceed via atypical mechanisms involving cell killing, it was judged that the threshold-like responses observed should not be generalized. Hormesis the possibility that low doses of radiation may have beneficial effects (a phenomenon often referred to as "hormesis") has been the subject of considerable debate. Although examples of apparent stimulatory or protective effects can be found in cellular and animal biology, the preponderance of available experimental information does not support the contention that low levels of ionizing radiation have a beneficial effect. At this time, the assumption that any stimulatory hormetic effects from low doses of ionizing radiation will have a significant health benefit to humans that exceeds potential detrimental effects from radiation exposure at the same dose is unwarranted. Identification of molecular mechanisms for postulated hormetic effects at low doses Definitive experiments that identify molecular mechanisms are necessary to establish whether Copyright National Academy of Sciences. Adaptive responses for radiation tumorigenesis have been investigated in quantitative animal studies, and recent information is suggestive of adaptive processes that increase tumor latency but not lifetime risk. However, these data are difficult to interpret, and the implications for radiological protection remain most uncertain. Tumorigenic mechanisms Further cytogenetic and molecular genetic studies are needed to reduce current uncertainties about the specific role of radiation in multistage radiation tumorigenesis; such investigations would include studies with radiation-associated tumors of humans and experimental animals. The review of cellular, animal, and epidemiologic or clinical studies on the role of genetic factors in radiation tumorigenesis suggests that many of the known strongly expressing cancer-prone human genetic disorders are likely to show an elevated risk of radiation-induced cancer, probably with a high degree of organ specificity. Cellular and animal studies suggest that the molecular mechanisms underlying these genetically determined radiation effects largely mirror those that apply to spontaneous tumorigenesis and are consistent with knowledge of somatic mechanisms of tumorigenesis. However, since major germline deficiencies in the genes of interest are known to be rare, it has been possible to conclude from published analyses that they are most unlikely to create a significant distortion of population-based estimates of cancer risk. A major theme developing in cancer genetics is the interaction and potential impact of more weakly expressing variant cancer genes that may be relatively common in human populations. The animal genetic data provide proof-of-principle evidence of how such variant genes with functional polymorphisms can influence cancer risk, including limited data on radiation tumorigenesis. Genetic factors in radiation cancer risk Further work is needed in humans and mice on gene mutations and functional polymorphisms that influence the risk of radiation-induced cancers. Where possible, human molecular genetic studies should be coupled with epidemiologic investigations. Revision of the Baseline Frequencies of Mendelian Diseases in Humans the baseline frequencies of genetic diseases constitute an important quantity in risk estimation. While there is no reason to consider revision of the baseline frequencies of congenital abnormalities (6%) and chronic diseases (65%), these two classes together constitute what are referred to as "mul- Copyright National Academy of Sciences. The prediction is that a new equilibrium between mutation and selection will be reached. The time it takes in terms of generations to attain the new equilibrium, the rate of approach to it, and the magnitude of increase in mutant (and disease) frequencies are dependent on the induced mutation rate, the intensity of selection, and the type of disease. In humans, the problem can be explored using genomic databases and knowledge of mechanisms of the origin of radiation-induced deletions to predict regions that may be particularly prone to such deletions. These predictions can subsequently be tested in the mouse, these tests can also provide insights into the potential phenotypes associated with such deletions in humans. With respect to epidemiology, studies on the genetic effects of radiotherapy for childhood cancer, of the type that have been under way in the United States and Denmark since the mid-1990s, should be encouraged, especially when they can be coupled with modern molecular techniques (such as array-based comparative genomic hybridization. These techniques enable one to screen the whole genome for copy number abnormalities.

The power of adaptive immune responses is due to their antigen specificity anxiety coach generic 25mg phenergan with mastercard, which we will be studying in the following chapters anxiety symptoms dsm phenergan 25mg generic. However anxiety symptoms before sleep safe phenergan 25mg, they harness anxiety 8 year old daughter order phenergan 25mg fast delivery, and also depend upon, many of the effector mechanisms used by the innate immune system, which we will describe in this chapter. The effector mechanisms that remove the infectious agent (for example, phagocytes and complement) are similar or identical in each phase, but the first two phases rely on recognition of pathogens by germline-encoded receptors of the innate immune system, whereas adaptive immunity uses variable antigen-specific receptors that are produced as a result of gene rearrangements. Adaptive immunity occurs late, because the rare B and T cells specific for the invading pathogen must undergo clonal expansion before they differentiate into effector cells that can clear the infection. Whereas the adaptive immune system uses a large repertoire of receptors encoded by rearranging genes to recognize a huge variety of antigens (see Section 1-10), innate immunity depends upon germline-encoded receptors to recognize features that are common to many pathogens. In fact, as we will see, the mechanisms of innate immunity discriminate very effectively between host cells and pathogen surfaces, and this ability to discriminate between self and nonself, and to recognize broad classes of pathogens, contributes to the induction of an appropriate adaptive immune response. In the first part of the chapter we will consider the fixed defenses of the body: the epithelia that line the internal and external surfaces of the body, and the phagocytes that can engulf and digest invading microorganisms. As well as killing microorganisms, the activities of some of these phagocytes induce the next phase of the early response, and ultimately, if the infection is not cleared, the adaptive immune response. The second part of the chapter is devoted to a system of plasma proteins known as the complement system. This important element of innate immunity interacts with microorganisms to promote their removal by phagocytic cells. Next, we take a closer look at the receptors used by the immune system to recognize pathogens, and the last part of the chapter describes how the activation of phagocytic cells at the beginning of the innate immune response to infection leads to the induced or adaptive immune response. Microorganisms that cause pathology in humans and animals enter the body at different sites and produce disease by a variety of mechanisms. Many different infectious agents can cause pathology, and those that do are referred to as pathogenic microorganisms or pathogens. Invasions by microorganisms are initially countered, in all vertebrates, by innate defense mechanisms that preexist in all individuals and act within minutes of infection. Only when the innate host defenses are bypassed, evaded, or overwhelmed is an induced or adaptive immune response required. In the first part of this chapter we will describe briefly the infectious strategies of microorganisms before examining the innate host defenses that, in most cases, prevent infection from becoming established. Thus we will look at the defense functions of the epithelial surfaces of the body, the role of antimicrobial peptides and proteins, and the defense of body tissues by macrophages and neutrophils, which bind and ingest invading microorganisms in a process known as phagocytosis. Infectious agents must overcome innate host defenses to establish a focus of infection. Our bodies are constantly exposed to microorganisms present in the environment, including infectious agents that have been shed from infected individuals. Contact with these microorganisms may occur through external or internal epithelial surfaces: the respiratory tract mucosa provides a route of entry for airborne microorganisms, the gastrointestinal mucosa for microorganisms in food and water; insect bites and wounds allow micro-organisms to penetrate the skin; and direct contact between individuals offers opportunities for infection of the skin and reproductive mucosa. The epithelial surfaces of the body serve as an effective barrier against most microorganisms, and are rapidly repaired if wounded. Furthermore, most of the microorganisms that do succeed in crossing the epithelial surfaces are efficiently removed by innate immune mechanisms that function in the underlying tissues. Thus in most cases these defenses, which we will examine in more detail in subsequent sections, prevent a site of infection from being established. It is difficult to know how many infections are repelled in this way, because there are no symptoms of disease. It is clear, however, that the microorganisms that a normal human being inhales or ingests, or that enter through minor wounds, are mostly held at bay or eliminated, since they seldom cause disease. Infectious disease occurs when a microorganism succeeds in evading or overwhelming innate host defenses to establish a local site of infection and replication that allows its further transmission. In other cases the infectious agent causes significant pathology as it spreads through the lymphatics or the bloodstream, or as a result of secreting toxins. Pathogen spread is often countered by an inflammatory response that recruits more effector molecules and cells of the innate immune system from local blood vessels. The induced responses of innate immunity act over several days while an adaptive immune response gets underway in response to pathogen antigens delivered to local lymphoid tissue. Such a response can target specific features of the pathogen and will usually clear the infection and protect the host against reinfection with the same pathogen.

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