Gotowe bibliografie tematyczne / Human immunodeficiency virus

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Gotowa bibliografia na temat „Human immunodeficiency virus”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 6 września 2023

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Artykuły w czasopismach na temat "Human immunodeficiency virus"

Lederman, Michael. "Haemophilia, human immunodeficiency virus and human immunodeficiency virus pathogenesis". Thrombosis and Haemostasis 104, nr 11 (2010): 911–14. http://dx.doi.org/10.1160/th10-02-0096.

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SummaryIn July 1982, the occurrence of three cases of acquired immunodeficiency syndrome (AIDS) in men with haemophilia was an immediate signal to Oscar Ratnoff that AIDS was transmissible through blood products. Work that he led provided important and clear indication that the AIDS agent was transmissible through pooled plasma products and had rapidly infected many men who had haemophilia. Before the blood supply was protected, the risk for infection in haemophilia was related directly to the intensity of therapy with pooled anti-haemophilic factor concentrates. Studies performed among the small proportion of haemophiliacs who remained uninfected despite heavy exposure to these plasma products revealed that the rare protective genotype – homozygosity for the 32 base pair deletion in the CCR5 gene was heavily concentrated in this population. Among those who did not have this protective genotype, a state of diminished immune activation distinguished these high risk uninfected haemophiliacs from haemophiliacs who later acquired human immunodeficiency virus (HIV) infection and from healthy uninfected controls. Immune activation state may not only predict risk for HIV acquisition but also appears to be an important predictor and likely determinant of HIV disease progression. The potential drivers of immune activation in chronic HIV infection include HIV itself, other co-infecting pathogens, homeostatic responses to cytopenia as well as the recently recognised phenomenon of translocation of microbial products across a damaged gut mucosal surface. This latter process is particularly compelling as clinical studies have shown a good relationship between indices of microbial translocation and markers of both immune activation and T cell homeostasis in chronic HIV infection. More recently, we have also found evidence that these microbial products also may drive a heightened tendency to thrombus formation in HIV infection via induction of monocyte tissue factor expression. Thus systemic exposure to microbial elements that are translocated through a gut mucosa damaged in the first few weeks of HIV infection may contribute to the pathogenesis of both immune deficiency and the heightened risk for vascular events that have been noted in persons with HIV infection.

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Tagawa, Miho. "4. Human Immunodeficiency Virus Associated Renal Dysfunction." Nihon Naika Gakkai Zasshi 100, nr 5 (2011): 1319–23. http://dx.doi.org/10.2169/naika.100.1319.

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Kamal, K. "Human Immunodeficiency Virus". Pediatrics in Review 26, nr 2 (1.02.2005): 67. http://dx.doi.org/10.1542/pir.26-2-67.

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Price, TW, SG DeMars, DL Palmer, MI Altman i JW Moore. "Human immunodeficiency virus". Journal of the American Podiatric Medical Association 80, nr 9 (1.09.1990): 510. http://dx.doi.org/10.7547/87507315-80-9-510.

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Kamal, Khalid. "Human Immunodeficiency Virus". Pediatrics In Review 26, nr 2 (1.02.2005): 67. http://dx.doi.org/10.1542/pir.26.2.67.

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Autran, Brigitte. "Human Immunodeficiency Virus". Expert Review of Vaccines 3, sup1 (sierpień 2004): S3—S4. http://dx.doi.org/10.1586/14760584.3.4.s3.

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DYKEMAN, MARGARET, KELLY FUGATE i SARAH LAU. "Human Immunodeficiency Virus". Nurse Practitioner 22, nr 3 (marzec 1997): 94???104. http://dx.doi.org/10.1097/00006205-199703000-00008.

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Brown, F. "Human immunodeficiency virus". Science 232, nr 4757 (20.06.1986): 1486. http://dx.doi.org/10.1126/science.3012776.

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Skinner, Anita. "Human immunodeficiency virus". Nursing Standard 31, nr 13 (23.11.2016): 64–65. http://dx.doi.org/10.7748/ns.31.13.64.s46.

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Phillips, David M. "Human Immunodeficiency Virus". New England Journal of Medicine 332, nr 4 (26.01.1995): 233. http://dx.doi.org/10.1056/nejm199501263320406.

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Rozprawy doktorskie na temat "Human immunodeficiency virus"

Wilson, Colleen. "Nurses with human immunodeficiency virus or acquired immunodeficiency syndrome". Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23974.

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This thesis will explore the various legal, administrative and ethical issues arising out of the situation in which nurse is HIV-positive or has AIDS. In contrast to the situation of patients suffering from AIDS or HIV, there has been little in the literature, whether legal or medical, on nurses who are infected. The rights and duties of these nurses, testing of nurses for the presence of HIV infection or AIDS and the issue of discrimination are among the matters discussed with reference to relevant legislation and ethical principles.

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Brettle, Raymond Patrick. "Human immunodeficiency virus : the Edinburgh epidemic". Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20883.

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For a variety of socio-economic reasons an epidemic of injection drug use (IDU) involving heroin occurred during the early 1980's in Edinburgh: one third were female, most were young, unemployed and living on large council estates. At the peak of this IDU epidemic, HIV arrived and rapidly spread through this community. By July 1989 over 1000 individuals or 0.1% of the population of Lothian (750,000) had been recognised to have been infected with HIV, the majority via IDU. This is of the same order as the worst affected region in England (North West Thames). The majority of these individuals however live in the City of Edinburgh with a population of only around 300,000 (1981 census). Consequently a realistic prevalence for this population is actually 0.3% or 3 times the worst affected English region. Thus this new area of medicine has considerable relevance for future medicine in Edinburgh and Scotland. The thesis describes the disease, the epidemiology of Injection Drug Use and IDU related HIV and the early epidemic in Edinburgh. It also describes the clinical services that were developed at the City Hospital in Edinburgh and the problems that this new service encountered. The provision of health care for this difficult patient population facilitated a variety of research projects. The thesis describes some of the results of these projects particularly those concerned with natural history, clinical presentation and use of antiretroviral therapy in IDU related HIV. Lastly the factors found to affect the transmission of HIV to the heterosexual partners of the patients are presented together with their relevance for other populations.

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Walker, S. M. "Transactivation of human immunodeficiency virus by human cytomegalovirus". Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387104.

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Cochrane, Alexandra. "Human immunodeficiency virus infection of CD8 lymphocytes". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/24468.

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To confirm that CD8 lymphocytes are infected with HIV in vivo, and to investigate the mechanism of infection, HIV long terminal repeat (LTR) DNA was quantified in CD8 lymphocyte subsets of known purity, isolated from the blood of 20 subjects with HIV infection. HIV LTR was demonstrated in CD8 lymphocytes of 18/20 subjects, and in the subjects with chronic infection the frequency of infection increased with disease progression. HIV infection of CD8^brightCD4^dim lymphocytes was significantly more frequent (median 1197 HIV LTR copies / million cells) than that of CD8+CD4- lymphocytes (undetectable in 7/9 subjects, p<0.01) suggesting infection on activation rather than during intrathymic development. The level of infection in the CD8^brightCD4^dim lymphocytes approached that in CD4 lymphocytes from the same subjects (median 3660 HIV LTR copies / million cells) and therefore could not be explained by CD4 lymphocyte contamination. Given the high level of infection of CD8^brightCD4^dim lymphocytes their prevalence and phenotype was assessed in 8 healthy and 16 HIV infected subjects. The proportion of CD8 lymphocytes with a CD8^brightCD4^dim phenotype ranged from 0.3 to 3.4% with no significant difference between HIV infected and healthy subjects. The majority displayed a CD45RA-ve CD27+ve (memory) phenotype, but in contrast to the populations generated in vitro, the circulating population was not uniformly activated but rather comprised both activated and quiescent cells. Thus HIV infected CD8 lymphocytes commonly circulate in HIV infected subjects, and are likely to be infected on activation rather than during intrathymic development. Given that a proportion of the circulating CD8^brightCD4^dim lymphocytes have a quiescent phenotype, they may act as a long lived reservoir with implications for viral eradication.

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Langeni, Delile Gertrude. "Self-Disclosure of Human Immunodeficiency Virus Status in Personal Relationships: Perceptions of South Africans Living with Human Immunodeficiency Virus". ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/4798.

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Despite enormous research on the experience of living with HIV, many questions remain regarding self-disclosure of HIV status to sexual partners by people living with HIV (PLWHIV), which is essential to reducing further infection. In this study, a phenomenological approach captured the experience of self-disclosure among South Africans living with HIV in Louwsburg, South Africa. The health belief model served as a theoretical framework, and in-depth interviews were conducted with 12 PLWHIV (8 women, 4 men) who self-disclosed their HIV status to their sexual partners. Their experiences were explored, discovering their illness, motives for self-disclosure, feelings regarding disclosing, responses of their sexual partners, their emotional reaction, and about their medical care. The themes rose from interviews showed that (a) many PLWHIV are reluctant to self-disclose until they actively experienced health issues; (b) motives for disclosure include the wish to ensure fairness; support and to empower other PLWHIV to prevent further infection; (c) feelings of disclosure are primarily relief and liberation, even though risks remain, especially for families separated by labor migration laws; (d) the response of sexual partners to disclosure varies widely; some are motivated to get tested and use condoms, decline and respond only with anger, blame, even abandonment; and (e) after accessing medical care, most PLWHIV reported support and appearing less sick, which reduces social stigma. The women were more open, forthcoming, and transparent about disclosing than men participants. Findings will assist with the creation of future health education programs aimed at creating safe environments to disclose HIV status, which may reduce community risk of contracting the virus.

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Loo, Ryan K. "Sampling Considerations in Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome Needs Assessments". DigitalCommons@USU, 2003. https://digitalcommons.usu.edu/etd/6179.

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The human immunodeficiency virus (HIV) reduces the number of healthy immune cells in the human body. When the immune cells drop below a certain level, the person is diagnosed as having acquired immunodeficiency syndrome (AIDS), which increases the likelihood of opportunistic infections. As a result, people living with HIV I AIDS (PL WH/ A) have an elevated need for medical and support services. HIV I AIDS needs assessments identify unmet needs, and the results are used in the allocation of resources. Failure to accurately identify needs due to nonrepresentative samples may result in PL WH/ A failing to receive needed services. Random sampling is rarely used, but convenience sampling may provide representative samples if the principles of generalization are followed. The purpose of this study was to assess the degree to which lack of representation is occurring, to assess the impact of lack of representation, and to explore ways to improve the representative qualities of a sample.

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Pise-Masison, Cynthia Ann. "Human Immunodeficiency Virus Type-1 Infection of Human Myeloid Cells". eScholarship@UMMS, 1994. https://escholarship.umassmed.edu/gsbs_diss/87.

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Infection with human immunodeficiency virus type 1 (HIV-1) results in a wide range of immunologic and hematopoietic abnormalities. The overall goal of this dissertation was directed toward obtaining a better understanding of the interactions of HIV-1 and myeloid cells in relation to the pathogenesis of AIDS. The human myelomonocytic cell line, HL-60, was used as a model system to determine if HIV-1 infects myeloid progenitor cells and subsequently, if infection affects their differentiation. HL-60 cells and the human prototypic T cell line, H9 were infected with three different HIV-l isolates (IIIB, PM213, and NL4-3) which are known to infect T cells. All three isolates productively infected both H9 and HL-60 cells; however, HIV-1 antigen expression and cytopathicity was delayed by approximately 15 days in infected HL-60 cells compared H9 cells. To examine the effect of HIV-l infection on myeloid differentiation, chronically infected HL-60 cells and clonal lines derived from them were induced to differentiate into either granulocytes by treatment with dimethyl formamide (DMF) or into monocytes by treatment with phorbol l2-myristate 13 acetate (PMA). By both cellular morphology and function, approximately the same percentage of treated, HIV-infected HL-60 cells differentiated into either granulocytes or monocytes as treated, control HL-60 cells. Taken together, these results indicate that HIV-1 infection does not affect the morphological or functional differentiation of HL-60 cells. In an effort to understand the differences in the regulation of HIV-l infection in myeloid versus T cells, the life cycle of NL4-3 was examined in HL-60 cells and H9 cells. Initially, NL4-3 replication was restricted in HL-60 cells compared to H9 cells. This restriction was overcome 15 days after infection by the generation of a viral isolate, NL4-3(M). NL4-3(M), harvested during the lytic phase of NL4-3 infection of HL-60 cells, caused cell death approximately 8 days after infection in both H9 and HL-60 cells. Although measurements of viral entry kinetics demonstrated that the timing of entry of NL4-3 and NL4-3(M) in HL-60 cells and NL4-3 in H9 cells was similar, a quantitative polymerase chain reaction (PCR) analysis of newly reverse transcribed NL4-3 DNA in H9 and HL-60 cells revealed that NL4-3 infected H9 cells and NL4-3(M) infected HL-60 cells contain consistently higher amounts of newly reverse transcribed DNA than NL4-3 infected HL-60 cells. The delay in NL4-3 replication in HL-60 cells was further amplified by inefficient spread of the virus throughout the HL-60 culture as measured by RNA production and DNA integration suggesting that another step in the viral life cycle after reverse transcription was also restricted. These results suggest that the efficiency of NL43 replication in HL-60 cells is restricted at several steps in the viral life cycle. Further, these restrictions are overcome by the generation of a viral variant, NL4-3(M), which efficiently replicates in myeloid cells. The tropism of NL4-3(M) was further characterized by testing its growth in monocyte-derived macrophages (MDM). Unlike NL4-3, NL4-3(M) productively infected MDM cultures. The ability of NL4-3(M) to infect macrophages was conferred by the envelope gene. This was demonstrated by the ability of the recombinant virus, NL4-3envA, which contains the envelope of NL4-3(M) in the context of the NL4-3 genome, to infect and replicate in MDM cultures. The envelope gene of NL4-3(M), however, did not confer ability to rapidly kill HL-60 cells. Together, these findings demonstrate that viral determinants controlling entry into MDM are different trom the determinants controlling the cytopathic phenotype in HL-60 cells.

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Shi, Ruili. "Biological studies on inhibitors of human immunodeficiency virus". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0024/NQ37913.pdf.

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McKiel, Vanessa. "Cytokine-induced alterations in human immunodeficiency virus multiplication". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55512.

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The ability of the human immunodeficiency virus (HIV) to replicate in T-cells and macrophages has been shown to be influenced by immunomodulatory cytokines; furthermore, HIV infection of these cells can alter the kinetics of cytokine transcription. We found that chronic HIV IIIB infection of myelomonoblastic PLB 985 cells resulted in an altered pattern of type 1 interferon (IFN) transcription. Paradoxically, despite the antiviral effects of IFN, HIV-induced dysregulation of IFN transcription may actually lead to the establishment of a cellular environment that supports a chronic infection.
Since HIV replication is dependent on cellular activation, immunosuppressive cytokines which deactivate T-cells and macrophages may be important modulators of an antiviral effect. We previously demonstrated the anti-HIV effects of IFN$ alpha$2, alone and in a cooperative combination with 3$ sp prime$-azido-2$ sp prime$3$ sp prime$-dideoxythymidine (AZT), in limiting the expression of HIV IIIB in promonocytic U937 cells. We further tested the anti-HIV potential of the immunosuppressive cytokines transforming growth factor beta (TGF-$ beta$1) and interleukin-10 (IL-10), alone and in combination with AZT. TGF-$ beta$1 as a single agent had no effect on the multiplication of HIV IIIB in de novo infected PLB 985 cells; however, co-treatment with TGF-$ beta$1 and AZT synergistically slowed virus multiplication within the first week following infection. The synergistic actions of TGF-$ beta$1 and AZT were also observed in PLB 985 cells infected with an AZT-resistant strain of HIV-1. In contrast, IL-10 seemed to enhance HIV IIIB multiplication in PLB 985 cells. These antiviral treatments had no inhibitory effect on HIV IIIB multiplication in the T-cell line Jurkat. Elucidation of the role of cytokines in controlling the degree of HIV multiplication may have an impact on both clinical treatments and understanding the progression to AIDS.

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Harrison, Thomas Stephen. "Interactions between Human Immunodeficiency Virus and Cryptococcus neoformans". Thesis, St George's, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299059.

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Książki na temat "Human immunodeficiency virus"

D, Richman Douglas, red. Human immunodeficiency virus. London: International Medical Press, 2003.

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Therapists, Canadian Association of Occupational. Position statement: Human immunodeficiency virus. Toronto: CAOT, 1990.

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LeGrice, Stuart, i Matthias Gotte, red. Human Immunodeficiency Virus Reverse Transcriptase. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7291-9.

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Lowe, John W. Human immunodeficiency virus research program. Frederick, Maryland: U.S. Army Medical Research, Development, Acquisition and Logistics Command (Provisional), 1993.

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Lowe, John W. Human immunodeficiency virus (HIV) research - AIDS. Fort Detrick, Maryland: Commander, U.S. Army Medical Research and Materiel Command, 1994.

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Redington, Bryce, i John W. Lowe. Human immunodeficiency virus (HIV) research (AIDS). Frederick, Maryland: Prepared for U.S. Army Medical Research and Development Command, 1993.

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London, Polytechnic of North. Information on the aids virus and human immunodeficiency virus infection. London: PNL, 1987.

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Organization, World Health, red. Prevention of sexual transmission of human immunodeficiency virus. Geneva: World Health Organization, 1990.

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Gerry, Bally, Gilmore Norbert i Canadian Medical Association, red. Counselling guidelines for human immunodeficiency virus serologic testing. Ottawa: Canadian Medical Association, 1993.

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Châteauvert, Michel. Counselling guidelines for human immunodeficiency virus serologic testing. Ottawa: The Canadian Medical Association, 1993.

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Części książek na temat "Human immunodeficiency virus"

Al-Hajjar, Sami. "Human Immunodeficiency Virus". W Textbook of Clinical Pediatrics, 1195–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_111.

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Harris, Rosemary. "Human Immunodeficiency Virus". W Essential Infectious Disease Topics for Primary Care, 167–86. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-034-2_10.

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Ranadive, Nikhil, Sophia A. Hussen i Rana Chakraborty. "Human Immunodeficiency Virus". W Sexually Transmitted Infections in Adolescence and Young Adulthood, 255–78. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-20491-4_17.

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Ramjit, Ruan T., i Angela M. Caliendo. "Human Immunodeficiency Virus". W Diagnostic Molecular Pathology in Practice, 253–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19677-5_31.

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Lamps, Laura W. "Human Immunodeficiency Virus". W Surgical Pathology of the Gastrointestinal System: Bacterial, Fungal, Viral, and Parasitic Infections, 153–56. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-0861-2_25.

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O’Shea, Daniel J. "Human Immunodeficiency Virus". W Encyclopedia of Immigrant Health, 854–58. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-5659-0_375.

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Scott, Nathan. "Human Immunodeficiency Virus". W Uveitis, 63–66. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-09126-6_7.

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Harr, Jeffrey N., Philip F. Stahel, Phillip D. Levy, Antoine Vieillard-Baron, Yang Xue, Muhammad N. Iqbal, Jeffrey Chan i in. "Human Immunodeficiency Virus". W Encyclopedia of Intensive Care Medicine, 1152. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1714.

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Toledano, Roulhac D. "Human Immunodeficiency Virus". W Consults in Obstetric Anesthesiology, 277–81. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59680-8_80.

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Stratton, Pamela. "Human Immunodeficiency Virus". W Clinical Perspectives in Obstetrics and Gynecology, 128–55. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2640-6_8.

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Streszczenia konferencji na temat "Human immunodeficiency virus"

Levine, P. H. "ACQUIRED IMMUNODEFICIENCY SYNDROME, HUMAN IMMUNODEFICIENCY VIRUS AND HEMOPHILIA". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644752.

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Less than 15 years ago the National Heart, Lung and Blood Institute surveyed physicians in the United States in order to characterize the demographics of hemophilia. The average age of persons with hemophilia in the United States was found to be 11.5 years old. By 10 years later, the life expectancy was predicted to be normal, and indeed the average age of persons with hemophilia in the U.S. is now in the early twenties. Early, intensive and predictably efficacious control of hemorrhage has made this result possible, and the therapeutic product which has allowed such control is commercial clotting factor concentrate.We now know that starting in 1978, and with great frquency during 1982 and 1983, the majority of U.S. hemophiliacs were infected with human immunodeficiency virus (HIV). It is estimated that as of January, 1987, approximately two thirds of the 20,000' persons with hemophilia in the United States have been infected with HIV. Among those with severe factor VIII deficiency, more than 9056 are seropositive. As of 1/5/87, there were 288 cases of AIDS among U.S. hemophiliacs, for an AIDS rate of approximately 2.256 of those with HIV infection. This number included 185 with severe, 32 with moderate and 28 with mild hemophilia A; 12 with severe, 6 with moderate and 1 with mild hemophilia B; 9 with vWD, and 4 others. A disproportionate number were older patients: 55 were ages 1-19; 62 ages 20-29; 85 ages 30-39, and 86 age 40 or older. Although the AIDS attack rate is no longer climbing logarhythmically, new cases are certainly still occurring.A variety of other HIV-related syndromes have emerged. Of great concern is immune thrombocytopenia, which is now relatively common; among a group of 209 carefully followed HIV-positive patients at our center, 31 (1556) are or have been thrombocytopenic. Progressive failure to normally gain height and weight in children with hemophilia has recently been shown by our group to correlate with HIV antibody positivity, and also with decreased T4/T8 ratio, decreased T4 cell count, decreased skin test reactivity, and subsequent development of ARC or AIDS in some such children. Finally, a picture of progressive fall in T4 count associated with recurrent non-specific infections and increased likelihood of positive viral culture, may predict an increased risk of developing AIDS.We know that the immune dysfunction in hemophilia is complex, and not wholly explained by HIV infection. One important factor may be the many foreign proteins contained in commercial clotting factor concentrates, and their ability to stimulate T cells. It is known that latent HIV infection in cultured T4 lymphocytes can be induced to enter the proliferative, viral secretory phase by the addition of soluble foreign antigens to the cell culture. Recent data of Brettler and colleagues, to be presented at this meeting, suggest that the use of highly purified VI!I:C (specific activity >3000 u/mg) in place of the present extremely impure products, may improve the immune dysfunction in hemophilia. This observation offers a new hypothetical approach to the prevention of progressive T4 cell depletion in HIV infected hemophiliacs, and requires immediate and extensive further study.The psychosocial burden of HIV infection is immense. The need for extensive, formal education and support programs is largely unmet in most parts of the world. Such programs are best run out of hemophilia treatment centers in most cases, and must include an active program on prevention of sexual transmission, provision of HIV testing before and during pregnancies, provision for maintenance of confidentiality, etc. Education concerning HIV is like all other forms of education. It requires formal organization, a curriculum, active rather than passive learning in which there is interaction between the teacher and the pupil, time for planned repetition, reinforcement with written materials, and assessment of goals achieved. For all of these reasons it is inappropriate to assume that the physician at the hemophilia center will be able to provide an adequate education program. Adquate paramedical personnel will need to undertake this effort, under the directjon of the physician.

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Torrens, Francisco, i Gloria Castellano. "Periodic Classification of Human Immunodeficiency Virus Inhibitors". W The 11th International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 2007. http://dx.doi.org/10.3390/ecsoc-11-01363.

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Druce, Megan, Paula Sommer, Philippe Le Mercier, Chantal Hulo, Patrick Masson i Tulio de Oliveira. "Human immunodeficiency virus (HIV) proteomics resource at BioAfrica". W BCB '15: ACM International Conference on Bioinformatics, Computational Biology and Biomedicine. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2808719.2811426.

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Gingo, Matthew R., Marjorie P. George, Lorrie Lucht, Cathy Kessinger, Barbara Rissler, Renee Weinman, William A. Slivka, Deborah McMahon, Frank C. Sciurba i Alison Morris. "Pulmonary Function In Human Immunodeficiency Virus Infected Individuals". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5201.

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Lellyawaty, Lellyawaty, Dhesi Ari Astuti i Yekti Satriyandari. "Pregnancy Experience of Mothers with Human Immunodeficiency Virus Infection". W The 6th International Conference on Public Health 2019. Masters Program in Public Health, Graduate School, Universitas Sebelas Maret, 2019. http://dx.doi.org/10.26911/the6thicph.03.07.

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Sapira, Violeta, Mihaiela Lungu, Alexandru Paul Baciu, Anca Telehuz, Constantin Marcu, Iulia Chiscop, Carmen Gavrila, Ciprian Dinu, Ginel Baciu i Anamaria Ciubara. "FROM DEPRESSION TO HUMAN IMMUNODEFICIENCY VIRUS – A CASE REPORT". W The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.19.

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Introduction: Human immunodeficiency virus (HIV) infection is often preceded or accompanied by neuropsychiatric symptoms, including depression. This fact has been evaluated in most of the clinical studies to date as associated with HIV infection already diagnosed. Case report: We report a case of a 46-year-old woman patient with no prior diagnosed pathology, suffering from depressive disorder for roughly 6 months, with a progressive evolution under treatment. Blood tests showed a moderate normochromic normocytic anemic syndrome of unspecified origin. Given the fact that depressive syndrome has not improved under treatment, a cerebral computed tomography (CT) scan and a cerebral magnetic resonance imaging (MRI) are decided, revealing an expansive cerebral process which in turn recommends performing stereotactic biopsy, but the family of the patient refuses the procedure. The patient is neurologically evaluated and after considering the cerebral MRI pattern and the presence of anemia, an HIV and syphilis detection test is decided, revealing a positive result for HIV infection. An antiretroviral therapy has been initiated, resulting in favorable clinical and imaging outcomes. Conclusions: Each patient and each case are individual and is to be approached as such. Depression in a progressive evolution under treatment requires imaging evaluation (cerebral CT scan, ideally cerebral MRI).

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Siregar, Masra Lena, i Robert Sinto. "Disseminated histoplasmosis in an untreated human immunodeficiency virus patient". W 11TH ANNUAL INTERNATIONAL CONFERENCE (AIC) 2021: On Sciences and Engineering. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0119359.

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Karagiannis, Dimitri, Verica Radisavljevic-Gajic i Hashem Ashrafiuon. "Control of Human Immunodeficiency Virus (HIV) Dynamics With Parameter Uncertainties". W ASME 2016 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/dscc2016-9755.

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This work considers a 3-state nonlinear model with two inputs for the controlled dynamics of the human immunodeficiency virus (HIV). The three states represent the number of healthy and unhealthy T-cells as well as the number of free virus particles in a person’s body. The two inputs represent two different types of anti-retroviral drugs that are available to treat a person infected with the virus. These inputs can be used to create a stable nominal point that is much healthier for the patient than the open-loop stable equilibrium point. The goal of this paper is to use the inputs, which are subject to constraints, to efficiently and accurately reach the desired nominal point despite parameter uncertainties. We have designed an integral sliding mode control law to achieve this goal, and simulations are presented to demonstrate the performance of the controller.

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Balakrishnan, Sivaraman, Oznur Tastan, Jaime G. Carbonell i Judith Klein-Seetharaman. "Communication interception of human signal transduction pathways by Human Immunodeficiency Virus-1". W 2009 IEEE International Workshop on Genomic Signal Processing and Statistics (GENSIPS). IEEE, 2009. http://dx.doi.org/10.1109/gensips.2009.5174369.

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Nugraha, Jaka, i Welly Nur Armawati. "Modelling on human immunodeficiency virus case using Poisson bivariate regression". W 2ND INTERNATIONAL CONFERENCE ON CHEMISTRY, CHEMICAL PROCESS AND ENGINEERING (IC3PE). Author(s), 2018. http://dx.doi.org/10.1063/1.5065060.

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Raporty organizacyjne na temat "Human immunodeficiency virus"

Lowe, John W., Francine McCutchan, John McNeil, Ellen Namie i Richard Daniella. Human Immunodeficiency Virus (HIV) Research - AIDS. Fort Belvoir, VA: Defense Technical Information Center, listopad 1994. http://dx.doi.org/10.21236/ada298062.

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Redington, Bryce C., i Martha B. Shaw. Human Immunodeficiency Virus (HIV) Research (AIDS). Fort Belvoir, VA: Defense Technical Information Center, luty 1991. http://dx.doi.org/10.21236/ada236988.

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Oldstone, Michael B. Proteins of Human Immunodeficiency Virus that Cross-React with Human 'Self' Antigens. Fort Belvoir, VA: Defense Technical Information Center, listopad 1991. http://dx.doi.org/10.21236/ada246936.

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Perlman, Daniel M., Neil M. Ampel, Ron B. Schifman, David L. Cohn i Charlotte M. Patton. Persistent Campylobacter Jejuni Infections in Patients Infected with Human Immunodeficiency Virus (HIV). Fort Belvoir, VA: Defense Technical Information Center, kwiecień 1988. http://dx.doi.org/10.21236/ada265459.

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Kennedy, Ronald C. Use of Synthetic Peptides Anti-Idiotypes for Controlling Human Immunodeficiency Virus Infection. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1992. http://dx.doi.org/10.21236/ada269558.

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Erling, Norrby, i Eva M. Fenyo. Human Immunodeficiency Virus (HIV) Infections: Strain and Type Variations; Diagnosis and Prevention. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 1991. http://dx.doi.org/10.21236/ada237815.

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Woloschak, G. E., J. Panozzo, C. R. Libertin i S. Schreck. Salicylic acid inhibits UV- and Cis-Pt-induced human immunodeficiency virus expression. Office of Scientific and Technical Information (OSTI), sierpień 1994. http://dx.doi.org/10.2172/10174895.

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Ennis, Francis A. Human Immune Responses to HTLV-III Virus Infections in the Acquired Immunodeficiency Syndrome. Fort Belvoir, VA: Defense Technical Information Center, październik 1987. http://dx.doi.org/10.21236/ada199059.

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Walls, Lichun H. Isolation and Preliminary Characterization of a Recombinant TAT Protein From Human Immunodeficiency Virus. Fort Belvoir, VA: Defense Technical Information Center, maj 1995. http://dx.doi.org/10.21236/ada298304.

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Ennis, Francis A. Human Immune Responses to HTLV-III Virus Infections in the Acquired Immunodeficiency Syndrome. Fort Belvoir, VA: Defense Technical Information Center, listopad 1988. http://dx.doi.org/10.21236/ada231412.

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