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Books on the topic 'Protesi mammaria'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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1

Hartley, James L., ed. Protein Expression in Mammalian Cells. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-352-3.

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2

Hacker, David L., ed. Recombinant Protein Expression in Mammalian Cells. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8730-6.

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3

Hauser, Hansjörg, and Roland Wagner, eds. Mammalian Cell Biotechnology in Protein Production. Berlin, New York: DE GRUYTER, 1997. http://dx.doi.org/10.1515/9783110809282.

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4

Ho, Sylvia. Chaperone-assisted protein disaggregation in the mammalian system. Ottawa: National Library of Canada, 2003.

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5

Protein expression in mammalian cells: Methods and protocols. New York: Humana Press, 2012.

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6

Grand, Roger John Alfred. The relationship of protein structure to function: Studies on mammalian and viral regulatory polypeptides. Birmingham: University of Birmingham, 1986.

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7

Kim, Sandra Ann. Attempts to express the regulatory domain of protein kinase C-alpha in mammalian cell lines. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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8

1959-, Gabai Vladimir L., ed. Heat shock proteins and cytoprotection: ATP-deprived mammalian cells. Austin, Tx: R.G.Landes, 1996.

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9

Kabakov, Alexander E. Heat shock proteins and cytoprotection: ATP-deprived mammalian cells. New York: Springer, 1997.

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10

(Editor), Hansjorg Hauser, and Roland Wagner (Editor), eds. Mammalian Cell Biotechnology in Protein Production. Walter de Gruyter, 1997.

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11

Wagner, Roland, and Hansj Hauser. Mammalian Cell Biotechnology in Protein Production. De Gruyter, Inc., 1997.

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12

Castro, Fidel O. Mammary Gland Transgenesis: Therapeutic Protein Production. Springer, 2013.

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13

1961-, Castro Fidel O., and Jänne Juhani, eds. Mammary gland transgenesis: Therapeutic protein production. Berlin: Springer, 1998.

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14

Alfred, Doig, ed. Protein therapeutics production : large-scale mammalian cell culture. Westborough, MA: DMD Publications, 2005.

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15

(Editor), Fidel O. Castro, and Juhani Jänne (Editor), eds. Mammary Gland Transgenesis: Therapeutic Protein Production (Biotechnology Intelligence Unit). Springer, 1998.

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16

Mikhailov, Alexei. Practical Fluorescence Microscopy in Mammalian Cells: Protein Localization and Function. Humana Press, 2008.

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17

1949-, Hauser Hansjörg, and Wagner Roland 1956-, eds. Mammalian cell biotechnology in protein production /editors, Hansjörg Hauser, Roland Wagner. Berlin: Walter de Gruyter, 1997.

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18

Peptides in Mammalian Protein Metabolism: Tissue Utilisation & Clinical Targetting (Portland Press Proceedings,). Ashgate Publishing, 1997.

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19

Roe, Simon, ed. Protein Purification Techniques. Oxford University Press, 2001. http://dx.doi.org/10.1093/oso/9780199636747.001.0001.

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Proteins are an integral part of molecular and cellular structure and function and are probably the most purified type of biological molecule. In order to elucidate the structure and function of any protein it is first necessary to purify it. Protein purification techniques have evolved over the past ten years with improvements in equipment control, automation, and separation materials, and the introduction of new techniques such as affinity membranes and expanded beds. These developments have reduced the workload involved in protein purification, but there is still a need to consider how unit operations linked together to form a purification strategy, which can be scaled up if necessary. The two Practical Approach books on protein purification have therefore been thoroughly updated and rewritten where necessary. The core of both books is the provision of detailed practical guidelines aimed particularly at laboratory scale purification. Information on scale-up considerations is given where appropriate. The books are not comprehensive but do cover the major laboratory techniques and common sources of protein. Protein Purification Techniques focuses on unit operations and analytical techniques. It starts with an overview of purification strategy and then covers initial extraction and clarification techniques. The rest of the book concentrates on different purification methods with the emphasis being on chromatography. The final chapter considers general scale-up considerations. Protein Purification Applications describes purification strategies from common sources: mammalian cell culture, microbial cell culture, milk, animal tissue, and plant tissue. It also includes chapters on purification of inclusion bodies, fusion proteins, and purification for crystallography. A purification strategy that can produce a highly pure single protein from a crude mixture of proteins, carbohydrates, lipids, and cell debris to is a work of art to be admired. These books (available individually or as a set)are designed to give the laboratory worker the information needed to undertake the challenge of designing such a strategy.
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20

St-Pierre, Benoit. Stra 13: An E-box repressor protein expressed in mammary epithelial cells. 2002.

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21

Fleming, Scott William. Characterizaton of an LSD-induced inhibitor of protein synthesis in the mammalian brain. 1986.

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22

Bascom, Roger Andrew. Identification, molecular and genetic characterization of a novel mammalian photoreceptor membrane protein (ROM1). 1994.

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23

Joshi, Purna A. Alx4, a stromally-restricted homeodomain protein, is required for normal mammary epithelial morphogenesis. 2006.

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24

Batt, Jane. Characterization of the role of protein tyrosine phosphatase sigma (PTP[sigma]) in mammalian development. 2002.

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25

Hope, James, and Mark P. Dagleish. Prion-protein-related diseases of animals and man. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0041.

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Scrapie, bovine spongiform encephalopathy (BSE), Creutzfeldt–Jakob disease (CJD), and related diseases of mink (transmissible mink encephalopathy), mule deer and elk (chronic wasting disease) are the founder members of a group of diseases called the transmissible degenerative (or spongiform) encephalopathies (TSE). These diseases can be transmitted by prions from affected to healthy animals by inoculation or by feeding diseased tissues. Prions are cellular proteins that can transfer metabolic and pathological phenotypes vertically from parent to progeny or horizontally between cells and animals. TSEs are characterised by the accumulation of the prion form of the mammalian prion protein (PrPC) in the central nervous system or peripheral tissues of animals and humans. Mutations of the human PrP gene are linked to rare, familial forms of disease and prion-protein gene polymorphisms in humans and other species are linked to survival time and disease characteristics in affected individuals. Iatrogenic transmission of CJD in man has occurred, and a variant form of CJD (vCJD) is due to cross-species transmission of BSE from cattle to humans. Atypical forms of scrapie and BSE have been identified during large-scale monitoring for TSEs worldwide. This chapter outlines our current understanding of scrapie, BSE, CJD and other TSEs and highlights recent progress in defining the role in disease of the prion protein, PrP.
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26

Clark, Bruce Douglas. Characterization of a heat shock protein synthesized in the mammalian retina following LSD-induced hyperthermia. 1987.

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27

Sabatinos, Sarah Anne. Investigation of the function of UV damaged DNA binding protein 1 (DDB1) in mammalian systems. 2005.

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28

Bagni, Claudia, and Eric Klann. Molecular Functions of the Mammalian Fragile X Mental Retardation Protein: Insights Into Mental Retardation and Synaptic Plasticity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0008.

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Chapter 8 discusses how Fragile X syndrome (FXS) is caused by the absence of the RNA-binding protein fragile X mental retardation protein (FMRP). FMRP is highly expressed in the brain and gonads, the two organs mainly affected in patients with the syndrome. Functionally, FMRP belongs to the family of RNA-binding proteins, shuttling from the nucleus to the cytoplasm, and, as shown for other RNA-binding proteins, forms large messenger ribonucleoparticles.
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29

Gabai, Vladimir L., and Alexander E. Kabakov. Heat Shock Proteins and Cytoprotection: Atp-Deprived Mammalian Cells. Springer, 2012.

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30

Uludag, Hasan. Microencapsulation of mammalian cells by an interfacial precipitation process: in vitro and in vivo cell survival and protein delivery. 1993.

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31

Gabai, Vladimir L., and Alexander E. Kabakov. Heat Shock Proteins and Cytoprotection: Atp-Deprived Mammalian Cells (Molecular Biology Intelligence Unit). Springer, 1996.

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32

Kramer, Carolyn, and Emily Blumberg. Immunosuppressants and Antiretroviral Therapy in HIV-Positive Transplant Patients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0028.

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Protease inhibitors (PIs), especially ritonavir, are inhibitors of CYP3A4 and P-gp1 and can significantly increase levels of calcineurin inhibitors and mammalian target of rapamycin (mTOR) inhibitors. Cobicistat is an inhibitor of CYP3A4, and its effect on levels of calcineurin inhibitors and mTOR inhibitors is likely to be similar to that of ritonavir. Efavirenz may result in lower concentrations of calcineurin inhibitors and mTOR inhibitors. Dose reduction and careful attention to monitoring drug levels are critical to avoid toxicity and maintain therapeutic immunosuppressive concentrations when PIs or cobicistat are coadministered with calcineurin inhibitors or mTOR inhibitors. Although there is no formalized recommendation for the ideal antiretroviral therapy regimen in HIV-positive transplant recipients, a regimen consisting of two nucleoside reverse transcriptase and an integrase inhibitor minimizes the risk of drug–drug interactions and simplifies dosing of immunosuppressive agents while maintaining a high barrier to resistance.
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33

Dixon, Bradley P., J. Christopher Kingswood, and John J. Bissler. Tuberous sclerosis complex renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0330.

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Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder affecting almost all organs. It has wider phenotypic variation than often appreciated, with less than half showing the combination of characteristic facial angiofibromas, epilepsy, and mental retardation. Renal angiomyolipomata or cysts are found in 90% and renal failure was historically a common mode of adult death from the disease. Pulmonary lymphangioleiomyomatosis is restricted to females. Angiomyolipomata or cystic disease, or both, may cause renal failure. Angiomyolipomata may also haemorrhage, especially from larger lesions. Manifestations of brain involvement substantially complicate management of many patients with TSC. The causative genes TSC1 and TSC2 encode tuberin and hamartin which are involved in control of the mammalian target of rapamycin pathway. Inhibitors of that pathway, such as sirolimus and everolimus, are therefore logical approaches to therapy and have been shown to be effective in reducing angiomyolipomata volume. It remains to be seen whether they can protect renal function.
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34

King, Carolyn M., Grant Norbury, and Andrew J. Veale. Small mustelids in New Zealand: invasion ecology in a different world. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198759805.003.0010.

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This chapter reviews the ecology of the three species of small mustelids introduced into New Zealand: the ferret (Mustela furo), the stoat (M. erminea) and the weasel (M. nivalis), for biological control of rabbits. New Zealand offers a mosaic of environments totally different from those in which the three species evolved, including a diminishing array of endemic fauna especially vulnerable to mammalian predators. Mustelids in New Zealand display significant adaptive flexibility in diet, habitat selection, co-existence, dispersal, body size, population biology and predatory impact, with results contrasting with those observable in their northern-hemisphere ancestors. These evolutionary and ecological responses by mustelids to new opportunities are of considerable interest to evolutionary ecologists, especially those interested in competition and predator-prey relationships. Likewise, the need to protect New Zealand’s native fauna has stimulated extensive research on alternative options for mitigating the effects of invasive predators, applicable to pest management problems in other countries.
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35

George, Grimble, and Backwell F. R. C, eds. Peptides in mammalian protein metabolism: Tissue utilization and clinical targeting : proceedings of the conference held at the Rowett Research Institute, Aberdeen, in September 1994. London: Portland, 1998.

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36

Glen, Alistair, and Christopher Dickman, eds. Carnivores of Australia. CSIRO Publishing, 2014. http://dx.doi.org/10.1071/9780643103177.

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The Australian continent provides a unique perspective on the evolution and ecology of carnivorous animals. In earlier ages, Australia provided the arena for a spectacular radiation of marsupial and reptilian predators. The causes of their extinctions are still the subject of debate. Since European settlement, Australia has seen the extinction of one large marsupial predator (the thylacine), another (the Tasmanian devil) is in danger of imminent extinction, and still others have suffered dramatic declines. By contrast, two recently-introduced predators, the fox and cat, have been spectacularly successful, with devastating impacts on the Australian fauna. Carnivores of Australia: Past, Present and Future explores Australia's unique predator communities from pre-historic, historic and current perspectives. It covers mammalian, reptilian and avian carnivores, both native and introduced to Australia. It also examines the debate surrounding how best to manage predators to protect livestock and native biodiversity. Wildlife managers, academics and postgraduate students will benefit from the most up-to-date synthesis by leading researchers and managers in the field of carnivore biology. By emphasising Australian carnivores as exemplars of flesh-eaters in other parts of the world, this book will be an important reference for researchers, wildlife managers and students worldwide. Winner of a 2015 Whitley Awards Certificate of Commendation for Zoological Text.
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37

D, Lonsdale-Eccles J., and International Laboratory for Research on Animal Diseases., eds. Protein traffic in parasites and mammalian cells: Proceedings of a workshop held at the International Laboratory for Research on Animal Diseases, Nairobi, Kenya, 29 August to 1 September 1988. Nairobi, Kenya: International Laboratory for Research on Animal Diseases, 1989.

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38

Bannister, John. Great Whales. CSIRO Publishing, 2008. http://dx.doi.org/10.1071/9780643096196.

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Whales are mysterious and fascinating creatures. Despite modern technology, their world is still largely unexplored and unknown. They can only be seen, or rather glimpsed, when they are near the sea surface, either from boats, or perhaps from shore, or underwater by divers. They also reach astonishing sizes – the blue whale, for example, can grow to 30 metres in length, equivalent to the height of a six-storey building, and can weigh more than 130 tonnes. Seven ‘Great Whales’ are found in the coastal waters surrounding Australia. These include six of the largest baleen whales – blue whale, fin whale, humpback whale, sei whale, Bryde’s whale and southern right whale – and the sperm whale, the largest toothed whale. This book provides a detailed account of these extraordinary mammals. As well as the seven Great Whales, a smaller species – the minke whale – is included because of its special interest to Australians. The book describes whales’ highly specialised mammalian structure and biology, and the history of people’s association with them, at first through legend and wonder, then whaling, and more recently whale watching. It also looks at their past and current status, and the conservation initiatives that are in place to protect them from existing or potential threats. With both historical and recent photographs, as well as an extensive glossary, Great Whales will be enjoyed by natural history enthusiasts, zoologists and students alike.
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39

Meng, X. J. Hepatitis E virus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0048.

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Hepatitis E virus (HEV) is a small, non-enveloped, single-strand, positive-sense RNA virus of approximately 7.2 kb in size. HEV is classified in the family Hepeviridae consisting of four recognized major genotypes that infect humans and other animals. Genotypes 1 and 2 HEV are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions, whereas genotypes 3 and 4 HEV infect humans, pigs and other animal species and are responsible for sporadic cases of hepatitis E in both developing and industrialized countries. The avian HEV associated with Hepatitis-Splenomegaly syndrome in chickens is genetically and antigenically related to mammalian HEV, and likely represents a new genus in the family. There exist three open reading frames in HEV genome: ORF1 encodes non-structural proteins, ORF2 encodes the capsid protein, and the ORF3 encodes a small phosphoprotein. ORF2 and ORF3 are translated from a single bicistronic mRNA, and overlap each other but neither overlaps ORF1. Due to the lack of an efficient cell culture system and a practical animal model for HEV, the mechanisms of HEV replication and pathogenesis are poorly understood. The recent identification and characterization of animal strains of HEV from pigs and chickens and the demonstrated ability of cross-species infection by these animal strains raise potential public health concerns for zoonotic HEV transmission. It has been shown that the genotypes 3 and 4 HEV strains from pigs can infect humans, and vice versa. Accumulating evidence indicated that hepatitis E is a zoonotic disease, and swine and perhaps other animal species are reservoirs for HEV. A vaccine against HEV is not yet available.
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40

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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