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Books on the topic 'Human cell types'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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1

El-Salam, Mahmoud Abd. The prevalence of different human papillomavirus types and p53 mutations in laryngeal squamous cell carcinomas. [s.l.]: typescript, 1994.

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2

Per, Höllsberg, and Hafler David A, eds. Human T-cell lymphotropic virus type I. Chichester: J. Wiley and Sons, 1996.

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3

Connor, Sabrina. Extraction of Human papillomavirus type 16 DNA from the SiHa cervical cancer cell line. Sudbury, Ont: Laurentian University, 1991.

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4

Mckhann, Guy Mead. Isolation and characterization of human T-cell lymphotropic virus type-1 from patients with tropical spastic paraparesis. [New Haven: s.n.], 1990.

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5

Verfasser, Schließmann Stephan J., Kirschbaum Andreas Verfasser, Plönes Till 1976 Verfasser, Müller-Quernheim Joachim 1953 Verfasser, Zissel Gernot Verfasser, Klinik für Pneumologie, Albert-Ludwigs-Universität Freiburg Medizinische Fakultät, and Albert-Ludwigs-Universität Freiburg, eds. Roflumilast-N-oxide induces surfactant protein expression in human alveolar epithelial cells type II. Freiburg: Universität, 2012.

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6

Swingler, Simon. Cytokine regulation of human immunodeficiency virus type 1 gene expression in cells of neural origin. [s.l.]: typescript, 1992.

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7

Bourgeault, Geoffrey A. Energy metabolism of wild type MCF-7 human breast cancer cells and its adriamyacin resistant derivative. Sudbury, Ont: Laurentian University, 1997.

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8

Gutowski, Nicholas Jan. Cellular and molecular studies related to a cell line of the oligodendrocyte-type-2 astrocyte lineage derived from a human glioblastoma multiforme. Birmingham: University of Birmingham, 1995.

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9

The immortal life of Henriette Lacks. Waterville, Me: Thorndike Press, 2010.

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10

The immortal life of Henrietta Lacks. New York: Crown Publishers, 2009.

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11

The Immortal Life of Henrietta Lacks. New York, USA: Broadway Paperbacks, 2011.

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12

Skloot, Rebecca. The Immortal Life of Henrietta Lacks. New York: Crown Publishers, 2009.

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13

The Immortal Life of Henrietta Lacks. New York: Crown Publishing Group, 2010.

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14

Skloot, Rebecca. The immortal life of Henrietta Lacks. New York: Broadway Paperbacks, 2011.

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15

Skloot, Rebecca. The immortal life of Henrietta Lacks. New York: Broadway Paperbacks, 2011.

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16

Skloot, Rebecca. The Immortal life of Henrietta Lacks. New York, USA: Crown Publishers, 2010.

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17

Skloot, Rebecca. The immortal life of Henrietta Lacks. New York: Crown Publishers, 2009.

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18

Skloot, Rebecca. The immortal life of Henriette Lacks. Waterville, Me: Thorndike Press, 2010.

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19

Skloot, Rebecca. The immortal life of Henriette Lacks. Waterville, Me: Thorndike Press, 2010.

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20

Skloot, Rebecca. The immortal life of Henrietta Lacks. Detroit: Large Print Press/Gale Cengage Learning, 2011.

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21

Read, Nick D. Fungal cell structure and organization. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0004.

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Human pathogenic fungi produce three basic ‘cell’ types: hyphae, yeast cells, and spores. The organization and subcellular structure of these different cell types and their modes of growth and formation are reviewed. Growth and form is the consequence of how new cell surface is formed. This is generated by the delivery of vesicles to the surface which provides new membrane and the enzymes for cell wall synthesis. To generate these various cell types, the pathway of vesicle secretion to the surface has to be carefully regulated. These vesicles have to be transported through the cell by the cytoskeleton, and in filamentous cells these vesicles accumulate at a supply centre called the Spitzenkörper before docking and fusion with the hyphal apex. Ultimately, membrane is also endocytosed and recycled behind actively expanding regions of the fungal surface. These various processes are described and particular emphasis is given to the structural and organizational features of fungal cells that play roles in their pathogenesis and virulence.
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22

Nat, Roxana, and Andreas Eigentler. Cell Culture, iPS Cells and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0013.

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Somatic reprogramming technology, which enables the conversion of adult human non-neural cells into neurons, has progressed rapidly in recent years. The derivation of patient-specific induced pluripotent stem (iPS) cells has become routine. The inherent broad differentiation potential of iPS cells makes possible the generation of diverse types of human neurons. This constitutes a remarkable step in facilitating the development of more appropriate and comprehensive preclinical human disease models, as well as for high throughput drug screenings and cell therapy. This chapter reviews recent progress in the human iPS cell culture models related to common and rare NDDs, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, spinal muscular atrophy, and degenerative ataxias. It focuses on the pathophysiological features revealed in cell cultures, and the neuronal subtypes most affected in NDDs. The chapter discusses the validity, limitation, and improvements of this system in faithfully and reproducibly recapitulating disease pathology.
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23

Benton, William H. Evaluation of mixed cell types and 5-Iodo-2' -Deoxyuridine treatment upon plaque assay titers of human enteric viruses. [Washington, D.C.? : U.S. Environmental Protection Agency], 1986.

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24

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
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25

Franceschi, Silvia, Hashem B. El-Serag, David Forman, Robert Newton, and Martyn Plummer. Infectious Agents. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0024.

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Eleven infectious agents (seven viruses, three parasites, and one bacterium) have been classified by the International Agency for Research on Cancer as carcinogenic to humans for one or more cancer sites: hepatitis B virus; hepatitis C virus; thirteen types of human papillomavirus (HPV); human immunodeficiency virus type 1 (HIV-1); human T-cell leukemia virus type 1; Epstein-Barr virus; Kaposi sarcoma herpesvirus; Helicobacter pylori; Opisthorchis viverrini; Clonorchis sinensis; and Schistosoma haematobium. Other infectious agents, such as Merkel cell polyomavirus, Plasmodium falciparum, and cutaneous HPVs, have been classified as “probably carcinogenic” or “possibly carcinogenic.” Accurate biomarkers of chronic infection have been essential for estimating risk and ascribing a causal role to infectious agents in cancer. Of the 14 million cases of cancer estimated to have occurred worldwide in 2012, 2.2 million were caused by infectious agents. Vaccination and screen-and-treat programs have the potential for greatly reducing the burden of cancer caused by infections.
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26

Hafler, David A., and Per H¿llsberg. Human T-Cell Lymphotropic Virus Type I. Wiley & Sons, Incorporated, John, 2009.

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27

Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.

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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
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28

Brennand, Kristen. Application of Stem Cells to Understanding Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0005.

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While much has been learned through clinical post-mortem and neuroimaging studies of patients and animal models of autism spectrum disorder (ASD), bipolar disorder (BD) and schizophrenia (SZ), these classical approaches have yet to fully elucidate the interaction of complex genetic risk factors on disease predisposition. The derivation of human induced pluripotent stem cells (hiPSCs) from patients with psychiatric disorders permits the study of the full complement of risk variants (known and unknown) that underlie disease predisposition, precisely in the cell types relevant to disease. The following chapter covers work to date regarding the advancements in the use of hiPSCs to model psychiatric disorders.
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29

Moriuchi, Hiroyuki. Human T-cell Lymphotropic Virus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0010.

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Human T-cell lymphotropic virus type 1 (HTLV-1), a human retrovirus that infects an estimated 10–20 million people worldwide, has endemic foci in Japan, West and Central Africa, the Caribbean, Central and South America, and Melanesia. Also, it is the etiological agent of a lymphoproliferative malignancy, adult T-cell leukemia/lymphoma (ATLL), as well as chronic inflammatory diseases such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 can be transmitted vertically, sexually, or by blood-borne transmission. ATLL occurs in approximately 5% of carriers who are infected during early childhood, and primary prevention is the only strategy likely to reduce this fatal disease. Children born to carrier mothers acquire the virus predominantly from breastfeeding. In endemic areas, mother-to-child transmission (MTCT) can be significantly reduced by screening pregnant women for the HTLV-1 antibody, followed by replacing breastfeeding with exclusive formula feeding. Indications for serological screening and recommendations for prevention of perinatal transmission are reviewed in this chapter.
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30

Muthukumar, Thangamani, Darshana Dadhania, Choli Hartono, and Manikkam Suthanthiran. Immunology, sensitization, and histocompatibility. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0279.

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Allograft rejection of the histo-incompatible allograft involves a highly orchestrated action of multiple cell types and mediators, with lymphocytes responsible for the identification of the foreignness of the allograft. The immune response directed against the donor is primarily, but not exclusively, directed at the donor’s major histocompatibility complex region class I and class II proteins. This chapter describes the immunobiology of the T cell and the role of human leucocyte antigens in clinical transplantation, thus identifying the targets for manipulation of the immune response by immune suppressants and through strategies designed to create a state of tolerance of the allograft.
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31

Monaco, Claudia, and Esther Lutgens. Atherosclerosis—a short history. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0010.

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The pathogenesis of human atherosclerotic lesions has long been debated and is still evolving nowadays. First conceptualized as chronically evolving degenerative disease initiating in the mother’s womb, then increasingly accepted as a dynamic process causing severe acute complications that jeopardize the blood flow to the heart. Evolution of the hypothesis mirrored the progress of cellular and molecular biology, leading to progressive broadening of the understanding of cell types and molecules involved in atherogenesis. This chapter describes the current histopathological view on the pathogenesis of atherosclerosis, and touches on a historical perspective weaving in the fundamental discoveries that still influence the perception of this disease in humans.
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32

Michels, Virginia V. Genetics. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0276.

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Genetic factors play a role in the development of many types of human disease. Genetic determinants may be chromosome abnormalities (Down syndrome, Kleinfelter syndrome, Turner syndrome), single gene defects (dilated and hypertrophic cardiomyopathies, Ehlers-Danlos syndrome, Marfan syndrome, neurofibromatosis, tuberous sclerosis, Gaucher disease, cystic fibrosis, sickle cell disease), mitochondrial mutations (MELAS, MERRF, Kearns-Sayre syndrome), or epigenetic or multifactorial factors. Genetics testing methods are also reviewed.
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33

Joyner, Alexandra, ed. Gene Targeting. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199637928.001.0001.

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Since the publication of the first edition of Gene Targeting: A Practical Approach in 1993 there have been many advances in gene targeting and this new edition has been thoroughly updated and rewritten to include all the major new techniques. It provides not only tried-and-tested practical protocols but detailed guidance on their use and applications. As with the previous edition Gene Targeting: A Practical Approach 2e concentrates on gene targeting in mouse ES cells, but the techniques described can be easily adapted to applications in tissue culture including those for human cells. The first chapter covers the design of gene targeting vectors for mammalian cells and describes how to distinguish random integrations from homologous recombination. It is followed by a chapter on extending conventional gene targeting manipulations by using site-specific recombination using the Cre-loxP and Flp-FRT systems to produce 'clean' germline mutations and conditionally (in)activating genes. Chapter 3 describes methods for introducing DNA into ES cells for homologous recombination, selection and screening procedures for identifying and recovering targeted cell clones, and a simple method for establishing new ES cell lines. Chapter 4 discusses the pros and cons or aggregation versus blastocyst injection to create chimeras, focusing on the technical aspects of generating aggregation chimeras and then describes some of the uses of chimeras. The next topic covered is gene trap strategies; the structure, components, design, and modification of GT vectors, the various types of GT screens, and the molecular analysis of GT integrations. The final chapter explains the use of classical genetics in gene targeting and phenotype interpretation to create mutations and elucidate gene functions. Gene Targeting: A Practical Approach 2e will therefore be of great value to all researchers studying gene function.
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34

Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.

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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.
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35

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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36

Araujo, Abelardo Q.-C. Neurological Manifestations of the Human T-lymphotropic Virus Type 1. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0161.

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The human T cell lymphotropic virus type 1 (HTLV-1) is a retrovirus that infects about 20 million individuals worldwide. Its typical neurological presentation is of a chronic, slowly progressive myelopathy named “HTLV-1-associated myelopathy/tropical spastic paraparesis” (HAM/TSP). HAM/TSP emerges as the tip of the iceberg among numerous other neurological clinical syndromes caused by this virus, such as inflammatory myopathies, polyneuropathies, ALS-like syndromes, dysautonomia, etc. HAM/TSP designates a spastic paraparesis with neurogenic bladder, and minor sensory signs. Pathologically, HAM/TSP is characterized initially by perivascular lymphocytic cuffing and mild parenchymal mononuclear infiltrates affecting mainly the thoracic spinal cord. This is followed by gliosis and scarring in later stages. The neuropathogenesis of HTLV-1 is still poorly understood but is apparently immune mediated. The therapy of TSP/HAM remains basically symptomatic.
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37

Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.

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Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.
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38

Frisch, Morten. Penile Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0055.

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Penile cancers are rare primary malignancies located on the glans, foreskin, or shaft of the penis, excluding the urethra. The vast majority of penile cancers are epithelial tumors representing histological subtypes of squamous cell carcinoma (SCC). Most penile SCCs are believed to develop through pre-invasive lesions known as penile intraepithelial neoplasia and penile carcinoma in situ. They account for 0.1%–0.3% of all incident cancers (excluding non-melanoma skin cancers) in the United States and other developed countries and up to 1% of all cancers in some countries in sub-Saharan Africa. Penile cancers are rare in men younger than 40 years, and are typically diagnosed among men above age 60. The two most important risk factors are pathological phimosis and infection with high-risk types of human papillomaviruses (HPV), both of which are preventable conditions.
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39

Raychaudhury, Amlanav. Structure and expression of a family of human type I epidermal keratin genes located on chromosome 17. 1988.

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40

Guidelines for preventing transmission of infection with human T-cell lymphotropic virus type III in the workplace: AIDS. [Olympia?]: Washington State Dept. of Social & Health Services, 1986.

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41

Grulich, Andrew E., Fengyi Jin, and I. Mary Poynten. Anal Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0037.

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Anal canal cancer is a generally uncommon cancer that has been increasing in incidence for several decades. In most geographic locations, squamous cell carcinoma (SCC) accounts for 70% or more of cases, and incidence is slightly higher in women than in men. The remaining cases are mainly adenocarcinoma, but the degree to which this represents misclassified rectal cancer is uncertain. In almost all cases, anal SCC is caused by persistent infection with high-risk types of human papillomavirus (HPV); HPV-16 accounts for 75% or more of all cases. Survival is highly stage-dependent, and cure is usual if the cancer is diagnosed early. The main risk factor is anal exposure to HPV, and for this reason homosexual men are at particularly high risk. In women, risk is increased in those with higher numbers of sexual partners, and in those with a history of HPV-related disease at genital sites.
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42

Lee, Gregory. Epitope/Peptide-Based Monoclonal Antibodies for Immunotherapy of Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0007.

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Two monoclonal antibodies, RP215 and GHR106, were selected, respectively, for the research and development of anti-cancer drugs targeting ovarian cancer and other types of human cancer. RP215 was shown to react with a carbohydrate-associated epitope located mainly in the variable regions of immunoglobulin heavy chains expressed on the surface of almost all cancer cells in humans. GHR106 was generated against a synthetic peptide corresponding to N1-29 amino acid residues in the extracellular domains of human GnRH receptor, which is surface-expressed by most cancer cells as well as the anterior pituitary. This monoclonal antibody was shown to serve as a bioequivalent analog to GnRH-derived decapeptides currently used clinically. The molecular mechanisms of action of these two antibody-based anti-cancer drug candidates were well elucidated following numerous biochemical, immunological, and molecular biological studies, mainly by using ovarian cancer as the model. Further preclinical studies with humanized forms of these two antibodies are essential.
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43

Modeling the risk of adult T-cell leukemia/lymphoma in persons infected with human T-lymphotropic virus Type I. [Bethesda, Md.?]: National Cancer Institute, Office of Cancer Communications, 1988.

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44

Roman, Eve, Alexandra Smith, and Lorelei Mucci. Leukemias. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0028.

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Leukemias are a diverse group of acute and chronic haematological malignancies, that account for 2% to 3% of cancers globally. Recent advances in molecular biology and therapy have transformed the landscape for several leukemia subtypes changing some, but by no means all, from rapidly fatal diseases to treatable conditions with a good prognosis. In general, however, this progress has not been matched by new aetiological insights. Albeit accounting for a relatively small proportion, genetic predisposition syndromes such as neurofibromatosis, Li-Fraumeni and Trisomy 21, have the biggest impact in children and young adults. At older ages, established chemical, physical and biological risk factors, which explain only a small proportion of the total disease burden, include chemotherapy for a preceding cancer, ionizing radiation, and the viral infections human T-cell lymphotropic virus type 1 (HTLV-1) which causes the rare adult T-cell leukemia/lymphoma (ATLL) and the human immunodeficiency virus (HIV) which is associated with an increased risk of acute lymphoid leukaemias. Workplace exposures to potential carcinogens such as benzene, butadiene, and styrene have also been linked to increased risk of leukemia.
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45

Drapeau, Elodie, Hala Harony-Nicolas, and Jacqueline N. Crawley. Animal and Cellular Models of Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0061.

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The study of childhood psychiatric disorders is especially challenging, not only because of the difficulties in obtaining relevant human samples but also because of ethical considerations regarding the ability of children to provide informed consent. Models that can be experimentally manipulated are therefore indispensable to study those disorders. Traditionally, biological psychiatry research has extensively employed animal models and characterizations of rodent behavior. More recently, induced pluripotent stem cells (iPSCs), and induced differentiation of iPSCs into different types of brain cells have offered new alternative strategies to elucidate mechanisms underlying cellular processes. Regardless of how they are created, optimal models should demonstrate face validity, construct validity, and predictive validity to be considered most relevant. This chapter highlights the major animal and cellular models currently used in the research of childhood-onset psychiatric disorders.
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46

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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47

Lorch, Mark. Biochemistry: A Very Short Introduction. Oxford University Press, 2021. http://dx.doi.org/10.1093/actrade/9780198833871.001.0001.

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Biochemistry: A Very Short Introduction discusses the key concepts of biochemistry, as well as the historical figures in the field and the molecules they studied. From bacteria to humans, all living things are composed of cells of one type or another, all of which have fundamentally the same chemistry. Biochemistry is the study of the chemical reactions within these cells; the molecules that are created, manipulated, and destroyed as a result of them; and the chemical structures such as DNA on which these biochemical reactions take place. This VSI considers the current science and innovations in the field. It also looks at the interaction between biochemistry, biotechnology, and synthetic biology.
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48

Money, Nicholas P. 4. Viruses. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199681686.003.0004.

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‘Viruses’ explains that millions of people die from interacting with viruses every year, but beyond the effects of viruses on human health, the lives of all organisms and the cycling of nutrients through the biosphere depend upon the activities of viruses. Viruses control populations of bacteria, archaea, and eukaryotes and this destructive power liberates massive quantities of nutrients in aquatic and terrestrial ecosystems. Viruses are organized into seven groups based upon the type of genome and its mechanism of replication. Viral genomes are encoded in single-stranded and double-stranded DNA and RNA molecules. The expression of viral genes occurs within infected cells utilizing the molecular machinery of the host.
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49

Ellam, Rob. 5. Physics heal thyself. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723622.003.0005.

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Stable and radioactive isotopes are used extensively in diagnostic and therapeutic medical applications including studies of human body composition, energy balance, protein turnover, and metabolism. ‘Physics heal thyself: isotopes in medicine’ shows how ionizing radiation is key to a host of medical imaging techniques with radioactive isotopes widely used to target and kill cancer cells. Enriched isotopes are used as biological tracers; doubly labelled water in the diagnosis of type 2 diabetes; and 13C-labelled urea in diagnosing stomach and duodenal ulcers. Medical uses of ionizing radiation are manifold including X-ray imaging, radiotherapy with external X-ray beams, brachytherapy, targeted radionuclide therapy, single photon emission computed tomography, and positron emission tomography.
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50

Kirchman, David L. Symbioses and microbes. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0014.

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The book ends with a chapter devoted to discussing interactions between microbes and higher plants and animals. Symbiosis is sometimes used to describe all interactions, even negative ones, between organisms in persistent, close contact. This chapter focuses on interactions that benefit both partners (mutualism), or one partner while being neutral to the other (commensalism). Microbes are essential to the health and ecology of vertebrates, including Homo sapiens. Microbial cells outnumber human cells on our bodies, aiding in digestion and warding off pathogens. In consortia similar to the anaerobic food chain of anoxic sediments, microbes are essential in the digestion of plant material by deer, cattle, and sheep. Different types of microbes form symbiotic relationships with insects and help to explain their huge success in the biosphere. Protozoa are crucial for wood-boring insects, symbiotic bacteria in the genus Buchnera provide sugars to host aphids while obtaining essential amino acids in exchange, and fungi thrive in subterranean gardens before being harvested for food by ants. Symbiotic dinoflagellates directly provide organic material to support coral growth in exchange for ammonium and other nutrients. Corals are now threatened worldwide by rising oceanic temperatures, decreasing pH, and other human-caused environmental changes. At hydrothermal vents in some deep oceans, sulfur-oxidizing bacteria fuel an entire ecosystem and endosymbiotic bacteria support the growth of giant tube worms. Higher plants also have many symbiotic relationships with bacteria and fungi. Symbiotic nitrogen-fixing bacteria in legumes and other plants fix more nitrogen than free-living bacteria. Fungi associated with plant roots (“mycorrhizal”) are even more common and potentially provide plants with phosphorus as well as nitrogen. Symbiotic microbes can provide other services to their hosts, such as producing bioluminescence, needed for camouflage against predators. In the case of the bobtail squid, bioluminescence is only turned on when populations of the symbiotic bacteria reach critical levels, determined by a quorum sensing mechanism.
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