Relevant bibliographies by topics / IMMUNODEFICIENZE

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'IMMUNODEFICIENZE'

Author: Grafiati
Published: 9 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "IMMUNODEFICIENZE"

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Giancane, Gabriella, Elisabetta Cortis, AnnaMaria Zicari, Paola Pansa, and Marzia Duse. "Dalle immunodeficienze alle malattie reumatologiche." Area Pediatrica 13, no. 3 (June 2012): 72–76. http://dx.doi.org/10.1016/j.arped.2011.09.001.

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Giancane, Gabriella, Elisabetta Cortis, Ilaria Ernesti, Annalisa Di Coste, and Marzia Duse. "Dalle immunodeficienze alle malattie reumatologiche." Area Pediatrica 13, no. 4 (October 2012): 111–16. http://dx.doi.org/10.1016/j.arped.2012.10.005.

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Azzari, Chiara. "Lo screening neonatale delle immunodeficienze severe combinate." Area Pediatrica 13, no. 1 (February 2012): 20–24. http://dx.doi.org/10.1016/j.arped.2012.03.007.

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AL Farsi, Tariq, Sanjeewani Weerakoon, Jalila Mohsin, Hussein Al Mashayakhi, Khawater Ahmed, Amal Al Maani, Khuloud Aboqusida, and Nashat Al Sukaiti. "Disseminated Cryptosporidiosis in an Infant with Non-HIV Pediatric Immunodeficiency: First Case Report from Oman." Oman Medical Journal 36, no. 6 (November 30, 2021): e326-e326. http://dx.doi.org/10.5001/omj.2021.44.

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Cryptosporidium is a rare but important pathogen, especially in children with immunodeficiency. Intestinal cryptosporidiosis is well described in immunocompetent and immunocompromised children, but respiratory and disseminated cryptosporidiosis in immunodeficient children is not often reported. We describe an Omani infant with disseminated cryptosporidiosis and failing pharmacological therapy in the context of severe combined immunodeficiency. Chronic diarrhea can be an initial symptom of immunodeficiency in the pediatric population. Awareness of cryptosporidiosis is critical to early detection and management for such patients. As antiparasitic agents are often ineffective, amelioration of immunosuppression in immunodeficient children should be a priority.
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Campisi, Paolo, Linda Vong, Jonathan M. Sgro, Nikolaus Wolter, Bo Ngan, and Jacob Friedberg. "Transcervical thymic biopsy in the immunodeficient child." LymphoSign Journal 6, no. 4 (December 1, 2019): 141–47. http://dx.doi.org/10.14785/lymphosign-2019-0014.

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Objective: The objectives of this study are to present a case series of immunodeficient children who underwent a transcervical thymic biopsy and to describe the transcervical approach to the thymus gland. Design: Case series. Setting: Pediatric otolaryngology practice in an academic setting. Patients: Consecutive sample of immunodeficient children (≤18 years old) who underwent thymic biopsies from 1996 to 2019 for the purpose of confirming or excluding profound T cell immunodeficiency. Intervention: Diagnostic transcervical thymic biopsy. Results: A total of 14 patients with atypical combined immunodeficiency underwent the procedure during the study period, with minimal post-operative complication. The thymus was found to be abnormal histologically in 9 children and normal in another 5 patients. In all cases, thymus morphology helped define the extent of the immunodeficiency, resulting in either supporting a decision to perform a bone marrow transplant (8 patients) or avoid this high risk procedure (3 patients). Conclusion: Thymus biopsy is helpful in the characterization of childhood immunodeficiency and provides critical information that affects the medical management. The transcervical approach to the thymus is feasible in children and can be accomplished with minimal morbidity. Statement of novelty: Biopsies of the thymus have assisted in the characterization of new entities of primary immunodeficiency.
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Ito, Yusuke, Kensuke Takaoka, Kazuhiro Toyama, Yoshitaka Wakabayashi, Aya Shinozaki-Ushiku, Aiko Okazaki, Kinuyo Chikamatsu, Satoshi Mitarai, Tetsuo Ushiku, and Mineo Kurokawa. "The First Case of Concomitant Mycobacterium genavense lymphadenitis and EBV-positive lymphoproliferative disorder." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (June 28, 2020): e2020035. http://dx.doi.org/10.4084/mjhid.2020.035.

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This is the first case of concurrent Mycobacterium genavense lymphadenitis and Epstein-Barr virus (EBV)-positive lymphoproliferative disorder (LPD) in the same lymph node with no immunocompromised history. M. genavense infection is a rare opportunistic infection mainly for human immunodeficiency virus (HIV)-infected patients. Although no immunodeficiency was detected in our patient, our case indicates that the immunodeficiency in the background of EBV latency type III and the immunosuppression by malignant lymphoma itself might induce the M. genavense lymphadenitis. This case highly alerts clinicians the immunosuppressive state of EBV-positive LPD with latency type III even if any serological immunodeficient factors are not detected.
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Burns, S. "Podiatric manifestations of AIDS." Journal of the American Podiatric Medical Association 80, no. 1 (January 1, 1990): 15–20. http://dx.doi.org/10.7547/87507315-80-1-15.

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Dermatologic, vascular, neurologic, and musculoskeletal complications are common among persons with acquired immunodeficiency syndrome (AIDS). These manifestations frequently involve the lower extremities and may be the initial presenting symptoms of human immunodeficiency virus (HIV) infection. It is important that practitioners of podiatric medicine be aware of these syndromes to facilitate early diagnosis of AIDS and to provide the best possible care for immunodeficient patients. The author provides a review of the manifestations of AIDS frequently encountered in podiatric practice, along with guidelines for treatment.
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Chalifoux, Laura V., Angela Carville, Douglas Pauley, Brendon Thompson, Andrew A. Lackner, and Keith G. Mansfield. "Enterocytozoon bieneusi as a Cause of Proliferative Serositis in Simian Immunodeficiency Virus–Infected Immunodeficient Macaques (Macaca mulatta)." Archives of Pathology & Laboratory Medicine 124, no. 10 (October 1, 2000): 1480–84. http://dx.doi.org/10.5858/2000-124-1480-ebaaco.

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Abstract Context.—Enterocytozoon bieneusi is the most frequent microsporidian parasite of human patients with acquired immunodeficiency syndrome and is a significant cause of diarrhea and wasting. Recently, this organism has also been recognized as a spontaneous infection of several species of captive macaques. As in humans, E bieneusi frequently causes enteropathy and cholangiohepatitis in immunodeficient simian immunodeficiency virus (SIV)–infected macaques. Objective.—To examine E bieneusi as an etiologic agent of nonsuppurative proliferative serositis in immunodeficient rhesus macaques (Macaca mulatta). Design.—Retrospective analysis of necropsy material obtained from immunodeficient SIV-infected rhesus macaques. Results.—Examination of SIV-infected rhesus macaques (n = 225) revealed E bieneusi proliferative serositis in 7 of 16 cases of peritonitis of unknown origin. The organism could be identified by in situ hybridization and polymerase chain reaction in sections of pleura and peritoneum obtained at necropsy. Serositis was always accompanied by moderate-to-severe infection of the alimentary tract, and morphologic evidence suggested dissemination through efferent lymphatics. Colabeling experiments revealed most infected cells to be cytokeratin positive and less frequently positive for the macrophage marker CD68. Sequencing of a 607–base pair segment of the small subunit ribosomal gene revealed 100% identity to sequences obtained from rhesus macaques (Genbank accession AF023245) and human patients (Genbank accession AF024657 and L16868). Conclusions.—These findings indicate that E bieneusi disseminates in immunodeficient macaques and may be a cause of peritonitis in the immunocompromised host.
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Hofmann, Adam, Gerasimos Zaharatos, and Mark Miller. "Case Report and Review of the Literature:Toxoplasma gondiiEncephalitis in a 40-Year-Old Woman with Common Variable Immunodeficiency and a New Diagnosis of Large Granular Lymphocytic Leukemia." Canadian Journal of Infectious Diseases and Medical Microbiology 19, no. 4 (2008): 309–10. http://dx.doi.org/10.1155/2008/614279.

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Toxoplasma gondiihas been well-documented to cause central nervous system infections in immunodeficient patients. The present study describes a case of central nervous system toxoplasmosis in a patient with common variable immunodeficiency and newly diagnosed large granular lymphocytic leukemia, with a review of the literature for this association.
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Ferreira Santos, Carla, Marlene Delgado, Ana Bárbara Simões, Joana Nunes, Isabel Pereira, and Orlando Gaspar. "Encefalite a Citomegalovírus em Doente com Vírus da Imunodeficiência Humana Negativa." Acta Médica Portuguesa 26, no. 5 (October 31, 2013): 608. http://dx.doi.org/10.20344/amp.4949.

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Secondary immunodeficiences are associated with an increased incidence of infection and malignancy, as well with development ofautoimmune disease. Immune system function is altered by many conditions, such as aging, malnutrition and mycobacterial infections. However, the treatment of the primary condition often results in the improvement of the immune compromise. The authors present a case of cytomegalovirus encephalitis and hepatitis, due to viral reactivation associated with development of secondary immunodeficience in an HIV-negative patient.
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Dissertations / Theses on the topic "IMMUNODEFICIENZE"

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CASCIANO, FABIO. "Aspetti immunologici di pazienti pediatrici con immunodeficienze primitive." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1278.

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La sindrome di DiGeorge (DGS) è causata da una delezione in emizigosi del locus 22q11.2 responsabile di difetti embriogenetici che determinano l’alterazione del timo e delle ghiandole paratiroidee, difetti cardiaci e anomalie facciali caratteristiche. In molti pazienti affetti da questa sindrome, il difetto immunitario è principalmente del compartimento T, sebbene siano state riportate anche anomalie quali disgammaglobulinemia, deficit di IgA e di cellule B della memoria. Sulla base dei dati immunologici, i pazienti DGS sono classificati in DGS completi (cDGS) e DGS parziali (pDGS): i cDGS corrispondono ad una rara forma di immunodeficienza grave combinata (0,5-1%), mentre i pDGS presentano una forma variabile di linfopenia T (da leggera a moderata). Dal punto di vista clinico, questi pazienti mostrano un ampio spettro d’infezioni insieme ad una disregolazione del sistema immunitario con manifestazioni atopiche e autoimmunitarie. I livelli cellulari T, sebbene ridotti, non sono predittivi del rischio di infezioni o autoimmunità. Le alterazioni della distribuzione del repertorio del recettore delle cellule T (TCR) e il ridotto apporto timico nei pazienti pDGS è stato variabilmente associato ad un maggior rischio di infezioni o autoimmunità. Per meglio definire alcuni aspetti della patogenesi e delle caratteristiche immunologiche, abbiamo studiato la cinetica della ricostituzione immunologica in una coorte di pazienti pDGS e in pazienti affetti da altre immunodeficienze primitive non direttamente riconducibili ad alterazioni del compartimento di cellule T (come pazienti con Malattia Granulomatosa Cronica - CGD). A tal fine sono state analizzate le cellule mononucleate del sangue periferico valutando: 1. Il fenotipo e le funzioni immunologiche tramite tecniche convenzionali. 2. La distribuzione del repertorio del TCR dei compartimenti cellulari T CD4+ e T CD8+ (TCRBV spectratyping). 3. L’immunofenotipo di maturazione delle cellule B. 4. La frequenza delle cellule nTreg. La correlazione tra il profilo immunologico in vitro e le caratteristiche cliniche può aiutare a chiarire alcuni aspetti della patogenesi e del difetto immunologico, al fine di identificare dei possibili indicatori di suscettibilità verso le infezioni o verso lo sviluppo di autoimmunità. Risultati e Discussione: I pazienti pDGS mostravano un ridotto numero di cellule T, sebbene non sia stata trovata una correlazione tra i bassi valori di cellule T e le infezioni ricorrenti. Il numero totale di cellule B nei pazienti pDGS e CGD era normale, sebbene sia stato osservato un significativo decremento di cellule B della memoria. La frequenza delle cellule T regolatorie naturali dei pazienti non mostrava differenze se confrontata con i valori dei controlli sani di pari età. La risposta linfoproliferativa verso ogni stimolo era statisticamente diminuita in tutti i pazienti. La distribuzione delle famiglie dei TCRBV è risultata perturbata, con maggiore rilevanza nelle cellule T CD8+ sia nei pazienti pDGS che in quelli CGD. In particolare, l’alterazione delle famiglie TCRBV ha mostrato una tendenza di normalizzazione nella distribuzione del repertorio delle cellule T (sia CD4+ che CD8+), come osservato anche in pazienti infetti da CMV. Le infezioni ricorrenti correlavano con una maggiore frequenza di alterazioni delle famiglie TCRBV nei pazienti pDGS ma non nei pazienti CGD. Sebbene nella sindrome DiGeorge i bassi valori di cellule T non siano predittivi delle infezioni, le maggiori alterazioni delle famiglie TCRBV, così come l’immunodeficienza umorale e la ridotta frequenza di cellule B della memoria CD27+, risultavano essere associati a un maggiore rischio di infezioni in questi pazienti. L’analisi dei pazienti CGD ha mostrato delle alterazioni significative sia nel compartimento cellulare T che in quello B, suggerendo che le alterazioni quantitative e qualitative trovate, possono contribuire alla eterogeneità del fenotipo clinico. Ulteriori studi sono necessari per delucidare come il sistema della NADPH ossidasi è coinvolto nell’alterazione immunologica dei pazienti CGD. In conclusione, le nostre analisi nelle PID hanno rilevato che altri compartimenti cellulari, oltre a quelli noti, possono essere coinvolti in queste malattie. Pertanto alcuni parametri come la distribuzione delle famiglie del TCRBV e la valutazione della maturazione delle cellule B dovrebbero essere usati come indicatori prognostici del rischio d’infezioni nel corso del follow-up per intraprendere eventuali terapie specifiche.
DiGeorge syndrome (DGS) is caused by a deletion in hemizygosis of 22q11.2 locus responsible for embryogenesis defects causing alterations of thymus and parathyroid glands, cardiac defects and abnormal facial features. In most patients, the immune defect is basically in T cell subset although abnormalities such as dysgammaglobulinemia, IgA and memory B cells deficiency have been also reported. On the basis of the immunologic findings, DGS patients are divided in complete DGS (cDGS), a rare form of severe combined immune deficiency (0.5-1%), and partial DGS (pDGS) presenting mild/moderate T cell lymphopenia. Clinically, these patients display a wide spectrum of infections together with a dysregulation of immune system as atopic and autoimmune manifestations. T cell levels, although reduced, are not predictive of the risk to develop infections or autoimmunity. The alterations of the T cell receptor (TCR) repertoire distribution and impaired thymic output in pDGS have been variably associated to a higher risk of infections or autoimmunity. In order to better define some aspects of the pathogenesis and immunological features we studied the kinetic of immune reconstitution in a cohort of pDGS patients and in patients affected by other primary immunodeficiencies not directly affecting T-cell compartments (as Chronic Granulomatous Disease patients) through peripheral blood mononuclear cells (PBMC) analysis of: 1. Phenotype and immunologic functions through standard techniques. 2. TCR repertoire distribution of T CD4+ and T CD8+ subsets (TCRVB spectratyping). 3. Immunophenotypic B-cell maturation. 4. Frequency of T regulatory cells. The correlation between the in vitro immunological profile and the clinical features might help to clarify some aspects of the pathogenesis of the immunological defects, in order to identify possible prognostic markers of increased risk of susceptibility to infections or of development of autoimmunity. Results and Discussion: pDGS patients exhibited decreased T-cell numbers, although no correlation was found between low T-cell values and recurrent infections. Total B-cell numbers in pDGS and CGD patients were normal, although a significantly decreased proportion of memory B cells was observed. No difference in natural T regulatory cells frequency was evident when compared with healthy controls in any groups. A statistical reduced lymphoproliferative response to stimuli (PHA, OKT3 and PWM) in all patients was observed. TCRBV family distribution resulted perturbed, with higher degree in CD8+ T-cell subset in both CGD and pDGS patients. Particularly, TCRBV family alterations in pDGS patients showed a trend of normalization in T cell repertoire distribution (both CD4+ and CD8+ T-cell), as observed in CMV congenital infected patients. Recurrent infections correlated with a high frequency of TCRBV family alterations in pDGS but not in CGD patients. Although low T-cell values were not predictive of recurrent infections in DiGeorge syndrome, higher TCRBV family alterations, as well as humoral immunodeficiency and reduced CD27+ B cell memory frequency, were associated to an increased risk of infections in these patients. Interestingly analysis of CGD patients showed significative alterations in both T and B cells compartments, suggesting that quantitative and qualitative alterations found, might contribute to the heterogeneity in the clinical phenotype. Further studies are needed to elucidate how NADPH oxidase system is involved in CGD patients immune alterations. In conclusion, our analysis on PID patients with well known defective cell compartments revealed that other subsets were also involved, therefore some parameters such as TCRBV family distribution and B-cell maturation could be used as further prognostic markers for follow-up and specific treatment.
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JACOB, AURELIEN MARC FLORENT. "IMPROVING TARGETED GENE EDITING IN HEMATOPOIETIC STEM CELLS FOR CLINICAL TRANSLATION." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/304800.

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Negli ultimi anni, l’editing genetico nelle cellule staminali/progenitrici ematopoietiche umane (HSPC) per il trattamento di malattie genetiche del sangue è migliorato drasticamente trasformando inserzioni genetiche casuali in precise e mirate modificazioni del genoma. La modifica mirata dei geni mutati ereditati consente la correzione in situ e la ricostituzione funzionale con il mantenimento del controllo endogeno dell'espressione. Recentemente abbiamo dimostrato che sia le rotture del DNA a doppio filamento indotte dall’editing che il genoma stesso dell’Adeno-Associated Virus 6 (AAV) innescano una risposta dipendente da p53 nell'HSPC che risulta in un ritardo della proliferazione con conseguente diminuzione della ricostituzione ematopoietica dopo il trapianto delle cellule editate in animali immuno-compromessi. Per cui, abbiamo quindi dimostrato come la soppressione di questa risposta mediante l’espressione transitoria della forma negativa dominante di p53 preservi la ricostituzione del lineage ematopoietico. Tuttavia, la biologia sottostante è rimasta sconosciuta, così come l'impatto dell'editing genetico sulle dinamiche clonali dell'HSPC modificate con riparo diretto per omologia (Homology Directed Repair, HDR) al momento del trapianto. Inoltre, lo stato quiescente delle HSC primitive costituisce un limite per l’editing genetico mediato da HDR, riducendo le sue possibili applicazioni cliniche. In questo lavoro, abbiamo prima superato tale limite esprimendo transitoriamente la proteina dell'adenovirus 5 E4orf6/7, che regola il principale controllore del ciclo cellulare, E2F, insieme alla nucleasi. Mediante un'analisi dell'espressione genica globale e mirata, abbiamo dimostrato come E4orf6/7 spinga le cellule in fase S/G2 con concomitante sovra-regolazione di tutti i principali componenti del macchinario HDR, aumentando così l'efficienza dell'inserimento del transgene in cellule precedentemente quiescenti. Nel contesto dello xenotrapianto, l'espressione combinata di E4orf6/7 e l'inibizione di p53 hanno migliorato l'efficienza del HDR (>50%) all'interno dell'innesto umano totale, superando i livelli riportati fino ad ora in letteratura. Tale risultato è stato riprodotto in diversi donatori da diverse fonti di HSPC e sono stati modificati più loci genomici, dimostrando la maggior versatilità di questa piattaforma se paragonata ad altre strategie di editing. In parallelo, abbiamo ideato una nuova tecnologia (BAR-seq) che consente il monitoraggio clonale di singole HSC modificate con HDR. Questo approccio prevede l’introduzione di un codice a barre ereditabile univoco (BAR) nel templato AAV6 necessario al HDR. Il sequenziamento ad alta copertura di tali sequenze negli xenotrapianti ha mostrato come l’editing genetico risulti in un attecchimento di pochi cloni dominanti. Mentre l'inibizione transitoria di p53 durante l’editing ha consentito un aumento sostanziale della composizione clonale dell'innesto senza alterare la capacità ripopolante delle HSC. Inoltre, questi dati suggeriscono come la risposta mediata da p53 sia responsabile di un'ematopoiesi oligoclonale. È importante sottolineare che il BAR-seq ha fornito la prima prova diretta che le HSC umane modificate con HDR mantengono un potenziale multilineage e subiscono più cicli di divisioni simmetriche e asimmetriche nei trapianti primari e secondari. In conclusione, auspichiamo che i miglioramenti messi a punto nel nostro protocollo di editing possano ampliare le possibili applicazioni cliniche dell’editing genetico.
The scope of genome engineering in hematopoietic stem/progenitor cells (HSPCs) has broadened from random to precise genome insertions for treating genetic diseases of the blood lineages. Targeted editing of inherited mutant genes allows in situ correction and functional reconstitution with preserved expression control. We recently showed that both the induced double-strand DNA breaks and the AAV6 genome trigger a p53-dependent DNA damage response in HSPC delaying proliferation and decreasing hematopoietic reconstitution after xenotransplantation. Suppression of this response by transient expression of a dominant negative p53 released cell-cycle block and rescued hematopoietic reconstitution. Yet, the underlying biology remained unknown as well as the impact of gene editing on clonal dynamics of HDR-edited HSPC upon transplantation. Moreover, it has long been contended that the quiescence of primitive HSC constrains HDR-mediated gene editing, thus limiting its perspective clinical applications in several diseases. Here, we first overcame such constraints by transiently expressing the adenovirus 5 protein E4orf6/7, which operates the major cell cycle controller E2F, together with the nuclease. By global and targeted gene expression analysis we showed engagement of targeted cells in S/G2 phases with concomitant upregulation of all major components of the HDR machinery, thus increasing the efficiency of targeted transgene insertion. Combined E4orf6/7 expression and p53 inhibition enhanced >50% HDR efficiency within human graft surpassing the levels reported until now in the literature. Such outcome was reproducible across several HSPC donors and sources, genomic loci and conceivably portable to most types of editing platforms. In parallel, we devised a novel technology (BAR-seq) which enables clonal tracking of individual HDR-edited HSC by introducing a unique heritable barcode in the AAV6 template. Deep sequencing of integrated BARs in human hematochimeric mice showed that only few (5-10) dominant clones of edited HSC robustly contributed to the hematopoietic graft long-term after transplant. Transient p53 inhibition during editing enabled substantial increase in polyclonal graft composition without altering individual HSC output, thus explaining the improved engraftment and highlighting the p53-mediated response as culprit of an otherwise oligoclonal hematopoiesis. Importantly, BAR-seq provided the first direct evidence that human HDR-edited HSC maintain multilineage potential and undergo multiple rounds of symmetric and asymmetric divisions in primary and secondary xenogeneic hosts. Altogether, we expect that the substantial gains obtained in HDR efficiency and polyclonal repopulation by our improved editing protocol should broaden applicability of HSC gene editing and pave its way to clinical translation.
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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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Chackerian, Bryce Charles. "Selection of simian immunodeficiency virus variants during progression to immunodeficiency /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/11492.

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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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Berglöf, Anna. "Models for infections in immunodeficiency /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-333-3/.

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White, Stephen Mark. "Assessing the impact of the Human Immunodeficiency Virus / Acquired Immunodeficiency Syndrome on Volkswagen of South Africa." Thesis, Port Elizabeth Technikon, 2001. http://hdl.handle.net/10948/40.

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This treatise takes the form of an impact study. It is based on a three-month period of research involving literature review, interviews with VWSA officers and a survey of 111 of the 5500 workers who comprised the workforce of the VWSA plant in Uitenhage at that time. The author has attempted to portray the general views of experts in the field of HIV/AIDS corporate impact and impact management. In addition he has attempted to assay the current and forecast policies and practices in respect of the management of the epidemic by VWSA. The workers in the plant were consulted by survey and a variety of insights into the level of understanding of the epidemic, tolerance levels, expectations and so on were made. The quantification of these insights must be viewed with caution since the survey sample of 111 was relatively low for a workforce of circa 5500. Calculations in respect of representativity are included to facilitate calculated caution. It has been shown that the HIV/AIDS epidemic has a considerable current impact on the company and that this impact can be expected to grow considerably in the future. It has been suggested that an active intervention program would be well timed if implemented immediately
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Wong, Gabriel K. "Haematopoietic clonality in common variable immunodeficiency." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6935/.

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The aetiology of Common Variable Immunodeficiency (CVID) has fascinated immunologists since Dr. Janeway reported the first case in 1953. While the advances in molecular biology have enlightened us on the aetiology in some patients, the majority is not caused by inherited genetic disorders. A convincing mechanism accounting for the intrinsic variable and partial nature of the condition has yet been proposed. CVID separates itself from other primary antibody deficiencies by the procurement of an abnormal T-cell compartment. Data from this study support that both T-cells and B-cells are subjected to similar deficiency. Investigation of the T-cell receptor repertoire by next-generation sequencing and multi-parametric flow cytometry suggests a severe reduction in naïve T-cell output from the thymus. Similarly, the study of long-lived plasma cell generation and survival highlighted the greatest functional deficits in the naïve B-cell pool, altogether supporting an acquired arrest in lymphogenesis. Using DNA methylation as a surrogate marker for pre-VDJ clonality, this study further shows that some CVID patients exhibited clonal haematopoiesis, adjoining CVID to other clonal haematopoiesis related acquired haematological disorders. Further work is being focused on using high resolution techniques to confirm this association and mechanistically define the development of antibody deficiency in adulthood.
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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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Mullighan, Charles Grenfell. "The immunogenetics of common variable immunodeficiency /." Title page, table of contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09MD/09mdm959.pdf.

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Books on the topic "IMMUNODEFICIENZE"

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1956-, Gluckman Jennifer C., and Vilmer E, eds. Acquired immunodeficiency syndrome. Amsterdam: Elsevier, 1986.

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Imperato, Pascal James, ed. Acquired Immunodeficiency Syndrome. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0807-2.

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Webster, A. D. B., ed. Immunodeficiency and Disease. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5.

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Letvin, Norman L., and Ronald C. Desrosiers, eds. Simian Immunodeficiency Virus. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78536-8.

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Rezaei, Nima, Asghar Aghamohammadi, and Luigi D. Notarangelo, eds. Primary Immunodeficiency Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-52909-6.

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Rezaei, Nima, Asghar Aghamohammadi, and Luigi D. Notarangelo, eds. Primary Immunodeficiency Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78936-9.

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International, Conference on AIDS (2nd 1986 Paris France). Acquired immunodeficiency syndrome. Amsterdam: Elsevier, 1986.

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Eva, Klein, ed. Acquired immunodeficiency syndrome. Basel: Karger, 1988.

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

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B, Webster A. D., ed. Immunodeficiency and disease. Dordrecht: Kluwer Academic Publishers, 1988.

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Book chapters on the topic "IMMUNODEFICIENZE"

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Barberis, Alberto, Chiara Azzari, Clementina Canessa, Francesca Lippi, and Marco De Carli. "Immunodeficienze Primitive." In Le malattie rare del sistema immunitario, 149–67. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5394-6_17.

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Pession, Andrea, and Lea Verlicchi. "Immunodeficienze congenite e acquisite." In Rianimazione in età pediatrica, 91–100. Milano: Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-2059-7_9.

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Gallottini, Marina. "Immunodeficiency." In Infectious Disease and Parasites, 171–73. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30009-2_1086.

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Scully, C., and S. R. Porter. "Immunodeficiency." In Immunological Aspects of Oral Diseases, 235–56. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4167-0_11.

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Louit, Aymeric, and Pedro C. Avila. "Immunodeficiency." In Challenging Cases in Allergy and Immunology, 303–22. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-443-2_20.

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Gooch, Jan W. "Immunodeficiency." In Encyclopedic Dictionary of Polymers, 900. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13990.

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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry, et al. "Immunodeficiency." In Encyclopedia of Molecular Mechanisms of Disease, 1038–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8927.

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Imperato, Pascal James. "Introduction." In Acquired Immunodeficiency Syndrome, 1–5. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0807-2_1.

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Altman, Ronald. "The epidemiology of AIDS in New Jersey." In Acquired Immunodeficiency Syndrome, 43–46. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0807-2_10.

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Ross, Michael W., and James A. Carson. "Effectiveness of distribution of information on AIDS." In Acquired Immunodeficiency Syndrome, 46–48. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0807-2_11.

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Conference papers on the topic "IMMUNODEFICIENZE"

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Levine, P. H. "ACQUIRED IMMUNODEFICIENCY SYNDROME, HUMAN IMMUNODEFICIENCY VIRUS AND HEMOPHILIA." In 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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Kamenetskaya, O. V. "Immunodeficiency disorders and treatment." In International Conference on Millimeter and Submillimeter Waves and Applications 1994. SPIE, 1994. http://dx.doi.org/10.1117/12.2303150.

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Kamenetskaya, O. V. "Immunodeficiency disorders and treatment." In Millimeter and Submillimeter Waves and Applications: International Conference, edited by Mohammed N. Afsar. SPIE, 1994. http://dx.doi.org/10.1117/12.183044.

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Statsi, M., and Y. Melnikova. "THE DEPENDENCE ON GENDER OF THE INCIDENCE OF FELINE VIRAL IMMUNODEFICIENCY AND FELINE VIRAL LEUKEMIA." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-91-93.

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The prevalence of feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) in the populations of domestic and homeless cats has been analyzed. The effectiveness of diagnostic methods used for the detection of feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) has been studied. It was found that the level of prevalence of viral diseases of cats, such as the immunodeficiency virus and the leukemia virus, depends on the lifestyle, gender, and health status of cats; the diagnosis of the immunodeficiency virus and the leukemia virus depends on the economic situation of the country and the commercial availability of test systems; Widespread vaccination has proven its effectiveness and the possibility of limiting the risks of infection. PCR is the gold standard in the diagnosis of viral diseases, but it is an expensive method.
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Dzhuvalyakov, Pavel, Dmitry Bogomolov, and Julia Zbrueva. "The relevance of the question of the study of a corpse with suspected HIV." In Issues of determining the severity of harm caused to human health as a result of the impact of a biological factor. ru: Publishing Center RIOR, 2020. http://dx.doi.org/10.29039/conferencearticle_5fdcb03a696517.02994233.

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HIV infection is a disease caused by the human immunodeficiency virus, characterized by acquired immunodeficiency syndrome, which contributes to the occurrence of secondary infections and malignant tumors due to deep inhibition of the body's protective properties. Today, the world is experiencing a pandemic of HIV infection, the incidence of the world's population, especially in Eastern Europe, is growing steadily.
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Malik, M. R. "Infection and Immunodeficiency in Down Syndrome." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1361.

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Mohammed, A., S. Mazher, A. Yelisetty, Y. Sheinin, R. A. Franco, and V. S. Ramalingam. "A Serious Complication of Common Variable Immunodeficiency." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1368.

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Maati, Moufagued, Vladimir V. Rozanov, and V. P. Avdoshin. "Immunodeficiency and laser magnetic therapy in urology." In ALT '96 International Symposium: Laser Methods for Biomedical Applications, edited by Alexander M. Prokhorov, Costas Fotakis, and Vladimir Pustovoy. SPIE, 1996. http://dx.doi.org/10.1117/12.257367.

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Torrens, Francisco, and Gloria Castellano. "Periodic Classification of Human Immunodeficiency Virus Inhibitors." In 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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Marcal, Iara Mateus, Ana Maria São Thiago Santiago Bez, Cristiana Danielle Guimarães Melo, Christiane Cota Vieira, Laura Carolina Vida Ferreira, Lucas Leonardo de Castro Borges, Luiz Severiano Ribeiro, and Matheus Fonseca Cardoso. "GOOD SYNDROME, A RARE TYPE OF IMMUNODEFICIENCY." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2094.

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Reports on the topic "IMMUNODEFICIENZE"

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

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

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Zheng, Ruo-xiang, Xun Li, Jing Li, Zhen-wei Liu, Feng Jiang, Nicola Robinson, and Jian-ping Liu. Does Chinese herbal remedy Tangcao tablet work for the treatment of HIV/AIDS：a systematic review of controlled clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0042.

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Review question / Objective: This study aims to evaluate the effectiveness and safety of Tangcao tablet (Tangcao) for treating people with HIV/AIDS. Condition being studied: Acquired immunodeficiency syndrome (AIDS) is a chronic infectious disease characterized by severe immunodeficiency caused by the human immunodeficiency virus (HIV). The infection attacks specifically the white blood cells, CD4+T (CD4) cells, weakening the immunity of individuals against infections such as tuberculosis. Without treatment, patients with AIDS may survive up to 2 years. Pneumocystis pneumonia and infections of the central nervous system are two of the most common causes of death in people with AIDS. AIDS still remains a significant global public health problem, with an estimated 37.7 million people infected with HIV at the end of 2020.
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Gardner, Murray B. Genetic Immunization for Lentiviral Immunodeficiency Virus Infection and Disease. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada361721.

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Gardner, Murray B. Genetic Immunization for Lentiviral Immunodeficiency Virus Infection and Disease. Fort Belvoir, VA: Defense Technical Information Center, November 1997. http://dx.doi.org/10.21236/ada338248.

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Libertin, C. R., S. Gavinski, and G. E. Woloschak. Evidence of T-cell abnormalities in immunodeficient wasted mice. Office of Scientific and Technical Information (OSTI), December 1991. http://dx.doi.org/10.2172/10173435.

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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, November 1991. http://dx.doi.org/10.21236/ada246936.

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Perlman, Daniel M., Neil M. Ampel, Ron B. Schifman, David L. Cohn, and Charlotte M. Patton. Persistent Campylobacter Jejuni Infections in Patients Infected with Human Immunodeficiency Virus (HIV). Fort Belvoir, VA: Defense Technical Information Center, April 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, August 1992. http://dx.doi.org/10.21236/ada269558.

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

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