Relevant bibliographies by topics / Hemic and Lymphatic Diseases

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

Academic literature on the topic 'Hemic and Lymphatic Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 March 2023

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Journal articles on the topic "Hemic and Lymphatic Diseases"

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Yang, Jue, Hui Song, Kun Cao, Jialei Song, and Jianjiang Zhou. "Comprehensive analysis of Helicobacter pylori infection-associated diseases based on miRNA-mRNA interaction network." Briefings in Bioinformatics 20, no. 4 (March 20, 2018): 1492–501. http://dx.doi.org/10.1093/bib/bby018.

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AbstractHelicobacter pylori (H. pylori) infection remains a cause of significant morbidity and mortality worldwide. Comprehensive understanding of the pathogenic mechanism of H. pylori and its interaction with host will contribute to developing novel prophylactical and therapeutical strategies. Here, we first determined microRNA (miRNA) levels in H. pylori-infected patients with gastritis, duodenal ulcer, gastric cancer or mucosa-associated lymphoid tissue lymphoma using miRNA data sets. Thirty-four differentially expressed miRNAs were identified and functional enrichment analysis of those miRNA target genes revealed that H. pylori infection were strongly associated with pathway in cancer and regulation of mRNA synthesis. Using disease connectivity analysis of 28 hub genes, we found that H. pylori may increase the risk of many extragastric diseases (e.g. cardiovascular disease, hemic and lymphatic diseases and nervous system disease). Altogether, our integrated analysis provided a new method to predict pathogen–human disease connectivity based on miRNA-mRNA interaction network and indicated anti-H. pylori therapy as an effective means of human diseases prevention.
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Bergan, John. "Venous and Lymphatic Diseases." Annals of Vascular Surgery 20, no. 6 (November 2006): 844. http://dx.doi.org/10.1007/s10016-006-9116-x.

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Raman, Siva P., Sudhakar N. J. Pipavath, Ganesh Raghu, Rodney A. Schmidt, and J. David Godwin. "Imaging of Thoracic Lymphatic Diseases." American Journal of Roentgenology 193, no. 6 (December 2009): 1504–13. http://dx.doi.org/10.2214/ajr.09.2532.

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Rada, F., Patricia Cristodor, and I. Rada. "Lymphatic overload and venous diseases." International Journal of Angiology 3, no. 01 (April 22, 2011): 70–76. http://dx.doi.org/10.1007/bf02014918.

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Liu, Xiaolei, and Guillermo Oliver. "New insights about the lymphatic vasculature in cardiovascular diseases." F1000Research 8 (October 29, 2019): 1811. http://dx.doi.org/10.12688/f1000research.20107.1.

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The heart contains a complex network of blood and lymphatic vessels. The coronary blood vessels provide the cardiac tissue with oxygen and nutrients and have been the major focus of research for the past few decades. Cardiac lymphatic vessels, which consist of lymphatic capillaries and collecting lymphatic vessels covering all layers of the heart, transport excess fluid from the interstitium and play important roles in maintaining tissue fluid balance. Unlike for the coronary blood vessels, until a few years ago, not much information was available on the origin and function of the cardiac-associated lymphatic vasculature. A growing body of evidence indicates that cardiac lymphatic vessels (lymphatics) may serve as a therapeutic cardiovascular target.
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Yamamoto, Takumi. "Various Lymphatic Reconstructive Surgeries Based on Pathophysiology of Lymphatic Vessel-related Diseases." Journal of Japanese College of Angiology 60, no. 5 (May 10, 2020): 61–66. http://dx.doi.org/10.7133/jca.19-00033.

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Dean, Malcolm. "Egypt conquers lymphatic filariasis." Lancet Infectious Diseases 4, no. 5 (May 2004): 260. http://dx.doi.org/10.1016/s1473-3099(04)01023-0.

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Xu, Wenjing, Natalie R. Harris, and Kathleen M. Caron. "Lymphatic Vasculature: An Emerging Therapeutic Target and Drug Delivery Route." Annual Review of Medicine 72, no. 1 (January 27, 2021): 167–82. http://dx.doi.org/10.1146/annurev-med-051419-114417.

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The lymphatic system has received increasing scientific and clinical attention because a wide variety of diseases are linked to lymphatic pathologies and because the lymphatic system serves as an ideal conduit for drug delivery. Lymphatic vessels exert heterogeneous roles in different organs and vascular beds, and consequently, their dysfunction leads to distinct organ-specific outcomes. Although studies in animal model systems have led to the identification of crucial lymphatic genes with potential therapeutic benefit, effective lymphatic-targeted therapeutics are currently lacking for human lymphatic pathological conditions. Here, we focus on the therapeutic roles of lymphatic vessels in diseases and summarize the promising therapeutic targets for modulating lymphangiogenesis or lymphatic function in preclinical or clinical settings. We also discuss considerations for drug delivery or targeting of lymphatic vessels for treatment of lymphatic-related diseases. The lymphatic vasculature is rapidly emerging as a critical system for targeted modulation of its function and as a vehicle for innovative drug delivery.
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Keiser, Paul B., and Thomas B. Nutman. "Update on lymphatic filarial infections." Current Infectious Disease Reports 4, no. 1 (January 2002): 65–69. http://dx.doi.org/10.1007/s11908-002-0069-0.

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Sapozhnikova, O. V., and E. E. Eliseeva. "Lymphatic self-massage for enhancing immunity during a pandemic." Academy of medicine and sports 2, no. 3 (December 18, 2021): 8–12. http://dx.doi.org/10.15829/2712-7567-2021-33.

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The article is devoted to the problem of improving immunity during the COVID-19 pandemic and the related effect of lymphatic self-massage.The article analyzes the general concepts of the lymphatic system and its functions, as well as lymphatic self-massage and its effect on cardiovascular and lymphatic systems.It is noted that the lymph flow stimulation through movements activates and normalizes the most important body functions. Using Skype, the authors surveyed medical students about knowledge on benefits and techniques of lymphatic selfmassage.Further, a master class was held on the technique of lymphatic self-massage. The authors studied the awareness of students about the benefits of lymphatic selfmassage, revealed a tendency to chronic diseases and assessed the benefits after the procedure.Based on the data obtained, it was revealed that viral infections, namely COVID-19, provoke one of the most common diseases — autoimmune thyroiditis. So, 64% of the respondents noted about it.Using lymphatic self-massage, the manifestations of this pathology decreases, the facial muscles relax and the blood and lymph outflow improves.Thus, there is an undoubted benefit of lymphatic self-massage for the prevention of diseases with immune involvement, including COVID-19.
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Dissertations / Theses on the topic "Hemic and Lymphatic Diseases"

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Luo, Alice, Joseph Maguire, Manisha Nukavarapu, and Ashokkumar Gaba. "Peeling away the layers to anemia." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/95.

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Anemia is a significant public health issue that affects a great number of people in developed and developing countries. The World Health Organization states when the Hb value is/dL in an adult male and/dL in a nonpregnant female, the individual is considered as anemic. Iron deficiency is one of the most common causes of anemia. Inadequate intake of iron, chronic blood loss, and/or a combination of both factors typically lead to iron deficiency anemia. In developed countries, chronic blood loss from gastrointestinal, genitourinary, and gynecological sources are the most common etiologies of iron deficiency anemia. Although there are reports of iron deficiency anemia leading to self-inflicted skin excoriation, there are few cases of chronic blood loss from skin excoriation resulting in severe iron deficiency anemia. We present a 49 year old female with significant past medical history of depression, anxiety and chronic back pain who presented after she was found to have profound anemia with hemoglobin of 4.1g/dl. During interviewing, she denied hematuria, hemoptysis, hematochezia, and had been without menstrual cycles for the past year. Urinalysis was negative for blood as well as two documented negative fecal occult blood tests. Iron studies completed showed severely reduced iron levels. Upon further interviewing, the patient reported a supposedly self-diagnosed keratin disorder. For the past ten years she has been self-treating the keratin disorder by applying topical tretinoin and then wrapping it in saran wrap. She would then peel off areas of skin over multiple areas of her body including all extremities and her face. Multiple pictures of bloody piles of tissue were shown. The patient required 3 units of packed red blood cells and was started on iron supplementation. Gastroenterology was consulted and agreed there was no GI source of her blood loss. Psychiatry further evaluated the patient and diagnosed her with obsessive-compulsive disorder with somatic delusions. The prevalence of anemia among chronic psychiatric patients is more frequent than general population. This coexistence deteriorates the quality of life of the patients, prolongs the psychiatric treatment period, and could even cause an increase in morbidity and mortality. Treatment-related factors, drugs taken, physical conditions, negative lifestyle habits, and nutritional disorders are the reasons for anemia among chronic psychiatric patients. Even though iron deficiency anemia in developed country is most often caused by chronic blood loss from gastrointestinal, genitourinary, and gynecological causes, it is important to evaluate for other factors when none of these are present. Psychiatric causes when warranted from history including somatic delusions from obsessive-compulsive disorder should be considered on the differential when other etiologies are less clear.
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Cromwell, Mary A. "The Role of T Lymphocytes in the hu-PBMC-SCID Mouse Model of Epstein-Barr Virus-Associated Lymphoproliferative Disease." eScholarship@UMMS, 1995. https://escholarship.umassmed.edu/gsbs_diss/158.

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Epstein-Barr virus (EBV) is associated with a spectrum of benign and malignant lymphoproliferative disorders, including acute infectious mononucleosis (IM), Burkitt's lymphoma (BL) and immunosuppression-associated B cell lymphoproliferative disease (LPD). Immunosurveillance mediated by virus-specific cytotoxic T lymphocytes is believed to protect immunocompetent hosts from EBV-associated lymphoma and LPD. Due to the lack of an adequate animal model, however, the precise immunologic mechanisms which provide this protection have not been directly demonstrated in vivo. Human peripheral blood mononuclear cell-reconstituted C.B.-17-scid/scid mice (hu-PBMC-SCID mice) develop EBV-positive LPD following intraperitoneal injection of PBMC from EBV-seropositive donors. The SCID mouse disease mirrors human EBV-associated LPD in morphology, presence of the EBV genome, clonality, and patterns of expression of latent viral cellular differentiation antigens. The hu-PBMC-SCID mouse provides a unique small animal model of EBV+ LPD, and it was used in this study to examine the role of CD8+ CTL in controlling LPD. Survival time increase significantly when EBV-specific cytotoxic T-cell lines (CTL) are adoptive transferred into hu-PBMC-SCID mice, demonstrating suppression of LPD in vivoby a CTL-mediated virus-specific mechanism. Survival time also increases significantly with administration of alloreactive CTL lines, suggesting that a non-virus-specific mechanism also contributes to control of EBV-associated LPD by CTL. NOD-SCID mice reconstituted with PBMC from donors with latent EBV infection develop EBV+ LPD with significantly less frequency than do C.B.17-SCID mice reconstituted with PBMC from the same donors. Administration of anti-CD8 mAb to these mice depletes human CD8+ cells and increases the incidence of LPD to 100%, demonstrating that CD8+ T cells are neccessary for protection from EBV-associated LPD. Adoptive transfer of human CD8+ T cells, but not CD4+ T cells, prevents LPD in CD8-depleted NOD-SCID mice. In vivo depletion of CD4+ T cells prevents engraftment of human T cells, and LPD does not develop in most mice after CD4+ cell depletion. These studies are the first to directly demonstrate both the protective role of CD8+ T cells and a requirement for CD4+ T cells in EBV -associated LPD in an in vivo model.
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Castaneda-Avila, Maira A. "The Role of a Monoclonal Gammopathy of Undetermined Significance Diagnosis in Healthcare Utilization." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1135.

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Background Monoclonal Gammopathy of Undetermined Significance (MGUS) is an understudied precursor of multiple myeloma (MM), the second most prevalent hematologic malignancy in the United States. This dissertation was designed to: (1) Describe the trajectories of serum biomarkers over time in patients with an MGUS diagnosis, (2) Determine if an MGUS diagnosis is associated with changes in healthcare service utilization, and (3) explore the patient- and provider-level drivers of healthcare utilization in patients with MGUS. Methods Data sources include health claims and electronic health records from a community-based population of patients seeking care in central Massachusetts and primary qualitative data collected from providers and patients’ interviews. The analyses included descriptive statistics, group-based trajectory modeling, conditional Poisson regression, and qualitative data analyses. Results (1) Three distinct multi-trajectory groups of creatinine and hemoglobin were identified. (2) The rates of emergency room, hospital, and outpatient visits were higher for patients with MGUS than patients without MGUS. (3) Patients have a basic understanding of MGUS; however, some patients feel anxiety, which may affect other aspects of their lives. Patients primarily see hematologists for follow-up care; other providers have less knowledge about MGUS. Conclusions Biomarker trajectories characterize specific subpopulations of patients with MGUS over time. We found that an MGUS diagnosis is associated with higher healthcare utilization, especially during the months surrounding the diagnosis date. Finally, our study suggests that some patients with MGUS may need psychosocial support services and identifies a gap in knowledge around caring for MGUS patients among primary care providers.
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Cullion, Kathleen J. "Mechanisms of NOTCH1 Mediated Leukemogenesis: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/537.

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Gain of function NOTCH1 mutations are common in both patients with T-ALL and in mouse models of the disease. Inhibiting the Notch pathway in T-ALL cell lines results in growth arrest and/or apoptosis in vitro, suggesting a requirement for Notch signaling in T-ALL. Therefore, we sought to examine the role of Notch1 signaling in both premalignancy and in the maintenance of leukemic growth. Using a murine model of T-ALL, in which expression of the Tal1 and Lmo2 oncogenes arrests thymocyte development, our preleukemic studies reveal that Notch1 mutations are early events that contribute to the clonal expansion of DN3 and DN4 progenitors. We also demonstrate that progenitors are maintained within the tumor and are enriched in leukemia-initiating cell (L-IC) activity, suggesting Notch1 may contribute to L-IC self-renewal. By studying the effects of Notch signaling in murine T-ALL cell lines, we also demonstrate that Notch1 promotes the proliferation and survival of leukemic blasts through regulation of Lef1 and the Akt/mTOR pathways. Given that T-ALL cell lines are dependent on Notch signaling in vitro, we investigated the effects of Notch inhibition in vivo. We provide evidence that Notch1 can be successfully targeted in vivo and that Notch inhibition, with γ-secretase inhibitors (GSIs), significantly extends the survival of leukemic mice. We also demonstrate that administration of GSIs in combination with rapamycin inhibits human T-ALL growth and extends survival in a mouse xenograft model. Given that NOTCH1 may be required to maintain both L-IC and bulk leukemic growth, targeting NOTCH1 may prove to be an efficacious targeted therapy for T-ALL patients with aberrant NOTCH1 activation.
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Nie, Siwei. "Role of TNF in Heterologous Immunity between Lymphocytic Choriomeningitis Virus and Vaccinia Virus: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/394.

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Prior immunity to a related or unrelated pathogen greatly influences the host’s immune response to a subsequent infection and can cause a dramatic difference in disease course, a phenomenon known as heterologous immunity. Heterologous immunity can influence protective immunity, immunopathology and/or immune deviation of cytokine-producing T cell subsets. Examples of heterologous immunity have been well documented in mouse models, as well as during human infections. For example, prior immunity to lymphocytic choriomeningitis virus (LCMV) provides partial protection against vaccinia virus (VV), as LCMV-immune mice show reduced VV titers and increased survival upon lethal dose VV infection. Heterologous protection against VV challenge, as a result of LCMV immunity, is mediated by LCMV-specific CD4 and CD8 T cells, as transfer of LCMV-specific memory T cells can mediate this protective effect in naïve mice. The recognition of a single TCR with more than one MHC-peptide complex is referred to as T cell cross-reactivity. A VV Kb-restricted epitope a11r198 was identified to be able to induce cross-reactive responses from LCMV-specific CD8 T cells. During VV infection, LCMV-specific memory T cells that are cross-reactive to VV epitopes produce IFN-γ early in VV infection. IFN-γ is essential for mediating the protection against VV in LCMV-immune mice, as this heterologous protection is absent in IFN-γR-/-and IFN-γ blocking antibody-treated LCMV-immune mice. In addition to protective immunity, cross-reactive LCMV-specific memory T cells and IFN-γ also induce an altered immunopathology during heterologous VV challenge. LCMV-immune mice show moderate to severe levels of inflammation of the fat tissue, known as panniculitis, in the visceral fat pads upon VV challenge. In humans, panniculitis is a painful condition, most commonly presenting as erythema nodosum. Erythema nodosum is a disease of unknown etiology with no known treatment. It may occur following intracellular bacterial and viral infections, and occasionally happens after vaccination with VV for smallpox. During infections there can be a delicate balance between the ability of immune responses to provide protective immunity, and the tendency to induce immunopathology. By using the mouse model of heterologous immunity between LCMV and VV, we tried to understand how the immunity to LCMV biased the balance between the protective immunity and immunopathology, and what effector molecules were responsible for the pathogenesis of panniculitis in this system. TNF is a pleiotropic cytokine, which is required for normal innate and adaptive immune responses. Its functions range from inducing proliferative responses including cell survival, to destructive responses such as promoting apoptosis and programmed necrosis. In response to inflammatory stimuli, activated macrophages/ monocytes produce large amounts of TNF, and upon activation, T cells, B cells and NK cells also produce TNF. In vitro and in vivo studies have shown that TNF in synergy with IFN-γ plays an important role in mediating host defense against pathogens, such as Listeria monocytogenesand poxviruses in mice and hepatitis B virus and human immunodeficiency virus in humans. However, inappropriate expression of TNF often results in tissue damage. Considering the important role TNF plays in both host defense and mediating autoimmune diseases, we hypothesized that TNF was required for mediating both protective and pathogenic effects in the heterologous immunity between LCMV and VV. We first examined whether TNF was involved in mediating protective heterologous immunity. LCMV-immune mice, that were TNF-deficient as a consequence of genetic deletion (TNF-/-) or receptor blockade by treatment with etanercept (TNFR2: Fc fusion protein), were challenged with VV. These TNF-deficient mice showed normal recruitment and selective expansion of cross-reactive LCMV-specific memory CD8 T cells. They also exhibited efficient clearance of VV similar to LCMV-immune mice with normal TNF function. Thus, we concluded that neither TNF nor lymphotoxin (LT), which uses the same receptors as TNF, was required in mediating protective heterologous immunity against VV. Indeed, prior immunity to LCMV could completely compensate for the role of TNF in protection of naïve mice against VV infection, even under conditions of lethal dose inoculum. Thus, heterologous immunity may help explain why treatment of humans with etanercept is reasonably well tolerated with relatively few infectious complications. One of the histological characteristics of panniculitis is necrosis of adipose tissue. It is known that three members in the TNF superfamily, i.e. TNF/LT, FasL and TRAIL are able to induce necrosis of a target cell. It is also known that TNF is able to induce VV-infected cells to go through necrosis, when apoptosis is blocked in these cells by VV protein. Furthermore, TNF and FasL have already been shown to be associated with some skin and fat pathology. Thus, we hypothesized that TNF, FasL and TRAIL were involved in the pathogenesis of panniculitis in VV infected LCMV-immune mice. By using blocking antibodies or genetically deficient mice, we demonstrated that both TNF/LT and FasL were crucial for inducing panniculitis. Although TNFR1 has been reported to induce programmed necrosis, our data indicated that TNFR2, not TNFR1, was involved in mediating tissue damage in the fat pads of LCMV-immune mice infected with VV. We also found that TNF signaled through TNFR2 to up-regulate the expression of Fas on adipocytes. Thus, the engagement of Fas on the adipocytes with FasL expressed on activated VV-specific and cross-reactive LCMV-specific CD8 T cells in the fat pads could lead to panniculitis. Thus, our data may identify a potential mechanism in the pathogenesis of human panniculitis, and may suggest a possible treatment for this painful disease. Recent reports suggest that heterologous immunity may contribute to the tremendous variation in symptoms between individuals, from subclinical to death, upon viral infection. Even in genetically identical mice, variations in immunopathology from none to life-threatening levels of pathology are observed in LCMV-immune mice during VV infection. By adoptive transfer of splenocytes from a single LCMV-immune donor into two recipients, we showed that similar levels of pathology were generated in mice receiving the same splenocytes. However, the level of pathology varied among recipients receiving splenocytes from different LCMV-immune donors. The difference in levels of VV-induced pathology observed in individual LCMV-immune mice was a reflection of the private specificity of the T cell repertoire, which is a unique characteristic of each individual immune host. The goal of this doctoral thesis is to understand how heterologous immunity contributes to the pathogenesis of panniculitis. Our data demonstrate that TNF/LT and FasL directly contribute to development of panniculitis in LCMV-immune mice during VV infection, and suggest that anti-TNF treatment might be a useful treatment for diseases, such as erythema nodosum and lupus-induced acute fatty necrosis in humans.
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Precopio, Melissa Lynn. "EBV-Specific CD4+ T Cell Responses in Acute Infectious Mononucleosis: a Dissertation." eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/113.

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Epstein-Barr virus (EBV) is a ubiquitous herpesvirus that establishes a life-long latent infection of B cells. It is usually asymptomatic in healthy individuals; however, individuals with compromised immunity often develop EBV-induced lymphoma. EBV also encodes potential oncogenes that can contribute to tumorigenesis. Therefore, vaccine and immunotherapeutic strategies targeting EBV are desirable. Recent studies have shown that infusion of EBV-specific CD8+T cells can elicit remission of lymphomas arising after administration of immunosuppressive drugs during transplantation, suggesting an important role for T cells in the prevention of EBV-induced malignancy. A better understanding of the cellular immune components involved in the control of EBV will aid in the development of methods to prevent infection and/or treat EBV-associated disease. While EBV infection is usually acquired asymptomatically during childhood, primary infection of adolescents and young adults can result in an illness termed acute infectious mononucleosis (AIM). Because of the characteristic symptoms of the illness, individuals with AIM can be readily identified and diagnosed with acute EBV infection. Thus, primary CD4+ and CD8+ T cell responses against the virus can be evaluated. It has been previously found that there is a marked expansion of lytic EBV protein-specific CD8+ T cells early during AIM, with delayed detection of lower frequencies of latent EBV protein-specific CD8+ T cells. The magnitude and specificity of CD4+T cell responses during AIM has been less well characterized. This thesis dissertation presents data from both functional assays and direct staining experiments documenting the timing, magnitude, and antigen-specificity of CD4+ T cells over the course of primary EBV infection. Lytic and latent protein-specific CD4+ T cells were readily detected by intracellular IFN-γ production at presentation with AIM and declined rapidly thereafter. Blood EBV load was also quantitated and found to decrease over time following AIM. By contrast, CD8+T cell IFN-y responses remained high for several weeks following presentation with AIM. Direct staining of lytic epitope-specific CD4+ T cells during AIM revealed high frequencies of virus-specific cells with low proliferative and IFN-γ-producing potential. Blood EBV load in these patients was persistently high through 6 wk following AIM. These data suggest a relationship between high EBV load during acute infection and impaired EBV-specific CD4+ T cell responses, which are compatible with impaired CD4+ T cell responses reported during high viremia associated with other viral infections. This may represent a mechanism by which persistent viruses, such as EBV, are able to establish a life-long infection in their hosts.
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Pan, Feng. "Understanding Ten-Eleven Translocation-2 in Hematological and Nervous Systems." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1925.

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I proposed the study of two distinct aspects of Ten-Eleven Translocation 2 (TET2) protein for understanding specific functions in different body systems. In Part I, I characterized the molecular mechanisms of Tet2 in the hematological system. As the second member of Ten-Eleven Translocation protein family, TET2 is frequently mutated in leukemic patients. Previous studies have shown that the TET2 mutations frequently occur in 20% myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN), 10% T-cell lymphoma leukemia and 2% B-cell lymphoma leukemia. Genetic mouse models also display distinct phenotypes of various types of hematological malignancies. I performed 5-hydroxymethylcytosine (5hmC) chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) of hematopoietic stem/progenitor cells to determine whether the deletion of Tet2 can affect the abundance of 5hmC at myeloid, T-cell and B-cell specific gene transcription start sites, which ultimately result in various hematological malignancies. Subsequent Exome sequencing (Exome-Seq) showed that disease-specific genes are mutated in different types of tumors, which suggests that TET2 may protect the genome from being mutated. The direct interaction between TET2 and Mutator S Homolog 6 (MSH6) protein suggests TET2 is involved in DNA mismatch repair. Finally, in vivo mismatch repair studies show that the loss of Tet2 causes a mutator phenotype. Taken together, my data indicate that TET2 binds to MSH6 to protect genome integrity. In Part II, I intended to better understand the role of Tet2 in the nervous system. 5-hydroxymethylcytosine regulates epigenetic modification during neurodevelopment and aging. Thus, Tet2 may play a critical role in regulating adult neurogenesis. To examine the physiological significance of Tet2 in the nervous system, I first showed that the deletion of Tet2 reduces the 5hmC levels in neural stem cells. Mice lacking Tet2 show abnormal hippocampal neurogenesis along with 5hmC alternations at different gene promoters and corresponding gene expression downregulation. Through the luciferase reporter assay, two neural factors Neurogenic differentiation 1 (NeuroD1) and Glial fibrillary acidic protein (Gfap) were down-regulated in Tet2 knockout cells. My results suggest that Tet2 regulates neural stem/progenitor cell proliferation and differentiation in adult brain.
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Shockett, Penny E. "Regulation of IgA Class Switch Recombination in the I.29μ B Cell Lymphoma by Cytokines and Inhibitors of Poly(ADP-ribose) Polymerase: A Thesis." eScholarship@UMMS, 1993. https://escholarship.umassmed.edu/gsbs_diss/133.

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Heavy chain isotype switch recombination is preceded by the appearance of RNA initiating 5' of the specific switch region which will undergo recombination. In an effort to understand the potential function of germline transcripts in switch recombination and the degree to which the regulation of germline transcripts correlates with the regulation of switching, we studied this process in the murine B-lymphoma cell line I.29μ, which in the presence of bacterial lipopolysaccharide (LPS) switches primarily to IgA and less frequently to IgE. Levels of α-germline transcripts initiating upstream of α switch (Sα) sequences are elevated in clones of this line which switch well as compared to clones which switch less frequently. TGFβ1 has been shown to increase α-germline transcripts and switching to IgA expression in LPS-stimulated murine splenic B-cells. We now demonstrate in I.29μ cells that TGFβ also increases switching to IgA and increases the level of α-germline transcripts 5 to 9 fold. Nuclear run-on analysis shows that this increase is at the level of transcription. Thus, TGFβ appears to direct switching to IgA by inducing transcription from the unrearranged Sα- CαDNA segment. Germline α RNA is quite stable in I.29μ cells, having a half life of about 3 to 5 hours, and we find only slight stabilization in the presence of TGFβ. Levels of ε-germline transcripts are not increased by TGFβ . IL-4, which modestly increases switching to IgA in I.29μ cells, slightly increases trancription of α-germline RNA. However, we present evidence suggesting that endogenously produced IL-4 may also act at additional levels to increase switching to IgA. IFNγ, which reduces IgA expression in these cells, also reduces the level of α-germline transcripts. IFNγ also reduces the level of ε-germline transcripts induced by IL-4. Our results support the hypothesis that the regulation of transcription of particular switch sequences by cytokines in turn regulates the specificity of recombination. In studies aimed at identifying other signalling pathways that promote class switching, we discovered that inhibitors of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) increase lipopolysaccharide (LPS)-induced switching to IgA in the B cell lymphoma I.29μ and to IgG1 in LPS + IL-4-treated splenic B cells. PARP, which binds to and is activated by DNA strand breaks, catalyzes the removal of ADP-ribose from NAD+ and poly(ADP-ribosylation) of chromatin-associated acceptor proteins. This enzyme is believed to function in cellular processes involving DNA strand breaks as well as in modulating chromatin structure. In I.29μ cells, PARP inhibitors increase IgA switching by day 2 and cause a 5-fold average increase in switching on day 3 as assayed by immunofluorescence microscopy. The PARP inhibitor, nicotinamide, also causes a reduced intensity of hybridization of Cμ and Cα specific probes to genomic DNA fragments containing the expressed VDJ-Cμ and the unrearranged Sα - Cα segments, respectively, indicating that PARP inhibition increases rearrangment of these fragments. Induction of switching by PARP inhibitors is not mimicked by treatment with cAMP analogs or reduced by inhibitors of protein kinase A (PKA). Induction of switching by PARP inhibitors does not appear to involve increased levels of transcription of the unrearranged Cα gene, although TGFβ is required for optimal induction by PARP inhibitors, consistent with a requirement for transcription of the unrearranged CH gene. PARP inhibitors do not overcome the requirement for endogenously produced IL-4.
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Litman, Rachel. "Characterization of the BACH1 Helicase in the DNA Damage Response Pathway: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/329.

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DNA damage response pathways are a complicated network of proteins that function to remove and/or reverse DNA damage. Following genetic insult, a signal cascade is generated, which alerts the cell to the presence of damaged DNA. Once recognized, the damage is either removed or the damaged region is excised, and the original genetic sequence is restored. However, when these pathways are defective the cell is unable to effectively mediate the DNA damage response and the damage persists unrepaired. Thus, the proteins that maintain the DNA damage response pathway are critical in preserving genomic stability. One essential DNA repair protein is the Breast Cancer Associated gene, BRCA1. BRCA1 is essential for mediating the DNA damage response, facilitating DNA damage repair, and activating key cell cycle checkpoints. Moreover, mutations in BRCA1 lead to a higher incidence of breast and ovarian cancer, highlighting the importance of BRCA1 as a tumor suppressor. In an effort to better understand how BRCA1 carried out these functions, researchers sought to identify additional BRCA1 interacting proteins. This led to the identification of several proteins including the BRCA1 Associated C-terminal Helicase, BACH1. Due to the direct interaction of BACH1 with a region of BRCA1 essential for DNA repair and tumor suppression, it was speculated that BACH1 may help support these BRCA1 function(s). In fact, initial genetic screenings confirmed that mutations in BACH1 correlated not only with hereditary breast cancer, but also with defects in DNA damage repair processes. The initial correlation between BACH1 and cancer predisposition was further confirmed when mutations in BACH1 were identified in the cancer syndrome Fanconi anemia (FA) (complementation group FA-J), thus giving BACH1 its new name FANCJ. These findings supported a previously established link between the FA and BRCA pathways and between FA and DNA repair. In particular, we demonstrated that similar to other FA/BRCA proteins, suppression of FANCJ lead to a substantial decrease in homologous recombination and enhanced both the cellular sensitivity to DNA interstrand cross-linking agents and chromosomal instability. What remained unknown was specifically how FANCJ functioned and whether these functions were dependent on its interaction with BRCA1 or other associated partners. In fact, we identified that FANCJ interacted directly with the MMR protein MLH1. Moreover, we found that the FANCJ/BRCA1 interaction was not required to correct the cellular defects in FA-J cells, but rather that the FANCJ/MLH1 interaction was required. Although both the FA/BRCA and MMR pathways undoubtedly mediate the DNA damage response, there was no evidence to suggest that these pathways were linked, until recently. Our findings not only indicate a physical link between these pathways by protein-protein interaction, but also demonstrated a functional link.
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10

Zhang, Haojian. "The Molecular Mechanisms for Maintenance of Cancer Stem Cells in Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/614.

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Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder associated with the Philadelphia chromosome (Ph) that arises from a reciprocal translocation between chromosomes 9 and 22, thereby resulting in the formation of the chimeric BCR-ABL oncogene encoding a constitutively activated tyrosine kinase. BCR-ABL tyrosine kinase inhibitors (TKIs) induce a complete hematologic and cytogenetic response in the majority of chronic phrase CML patients. However, TKIs cannot efficiently eradicate leukemia stem cells (LSCs) because of the insensitivity of LSCs to TKIs. Therefore, developing new strategies to target LSCs is necessary and critical for curing CML, and success of this approach depends on further understanding the molecular mechanisms by which LSCs survive and are maintained. In Chapter I, I briefly introduce CML disease, BCR-ABL oncoprotein, and TKIs. I also describe the identification and features of LSCs. Several key pathways in LSCs including Wnt/ß-catenin, hedgehog, FoxO, Bcl6 and HIF1, are discussed. I also propose our strategy to identify unique molecular pathways that are important for LSCs but not their normal stem cell counterparts. In Chapter II, I describe our finding about the function of the positive regulator, HIF1α, in CML development and LSC survival. I show that loss of HIF1α impairs the maintenance of CML through impairing cell cycle progression and inducing apoptosis of LSCs, and I also report that p16Ink4a and p19Arf mediate the effect of HIF1α on LSCs, as knockdown of p16Ink4a and p19Arf rescues the defective colony-forming ability of HIF1α-/- LSCs. As detailed in Chapter III and IV, through comparing the global gene expression profiles of LSCs and HSCs, I find two novel regulators, Blk and Scd1, which act as tumor suppressors in CML development. In Chapter III, I show that Blk is markedly down-regulated by BCR-ABL in LSCs, and that c-Myc and Pax5 mediate this down-regulation. Deletion of Blk accelerates CML development; conversely, Blk overexpression significantly delays the development of CML and impairs the function of LSCs. I also demonstrate that p27, as a downstream effector, is involved in the function of Blk in LSCs. Blk also functions as a tumor suppressor in human CML stem cells, and inhibits the colony-forming ability of human CML cells. In Chapter IV, I investigate the function of another negative regulator, Scd1, in CML LSCs, and find that expression of Scd1 is down-regulated in mouse LSCs and human CML cells. We report that Scd1 acts as a tumor suppressor in CML, as loss of Scd1 causes acceleration of CML development and overexpression of Scd1 delays CML development. Using a colony-forming assay, I demonstrate that Scd1 impairs the maintenance of LSCs due to the change of expression of Pten, p53 and Bcl2. Importantly, I find that both Blk and Scd1 do not affect normal hematopoietic stem cells (HSCs) or hematopoiesis. Taken together, our findings demonstrate that HIF1α is required for the maintenance of CML LSCs, and conversely that Blk and Scd1 suppress the function of LSCs, suggesting that combining TKI treatment with specific targeting of LSCs will be necessary for curing CML.
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Books on the topic "Hemic and Lymphatic Diseases"

1

Nicos, Labropoulos, and Stansby Gerard, eds. Venous and lymphatic diseases. New York: Taylor & Francis, 2006.

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B, Nutman Thomas, ed. Lymphatic filariasis. London: Imperial College Press, 2000.

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G, Rockson Stanley, ed. The lymphatic continuum revisited. Malden, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2008.

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K, White Elizabeth, ed. Hematology, the lymphatic system, and the immune system. 3rd ed. Englewood Cliffs, N.J: Regents/Pentice Hall, 1993.

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International, Congress of Lymphology (18th 2001 Genoa Italy). Progress in lymphology--XVIII: Proceedings of the 18th International Congress of Lymphology, September 3-7, 2001, Genoa, Italy. [S.l: s.n.], 2002.

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Mitsumasa, Nishi, Uchino Shigeo, and Yabuki Soh, eds. Progress in lymphology--XII: Proceedings of the XIIth International Congress of Lymphology, held in Tokyo, Kyoto, Japan, 27 August - 2 September 1989. Amsterdam: Excerpta Medica, 1989.

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1987, Mannheimer E. d., Kaindl F, and Partsch H, eds. Progress in lymphology--XI: Proceedings of the XIth International Congress of Lymphology, held in Vienna, Austria, 24-27 September 1987. Amsterdam: Excerpta Medica, 1988.

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M, Földi, Földi E, and Kubik S, eds. Foldi's textbook of lymphology for physicians and lymphedema therapists. 2nd ed. München, Germany: Elsevier GmbH, Urban & Fischer Verlag, 2006.

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Lymphatic filariasis, the disease and its control. Geneva: World Health Organization, 1992.

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Hildegard, Wittlinger, ed. Introduction to Dr. Vodder's Manual Lymph drainage: Vol. 1: Basic Course. 2nd ed. Heidelberg: Haug, 1985.

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Book chapters on the topic "Hemic and Lymphatic Diseases"

1

Fowler, Murray E., and P. Walter Bravo. "Hemic and Lymphatic Systems." In Medicine and Surgery of Camelids, 407–22. Ames, Iowa USA: Blackwell Publishing, Inc., 2013. http://dx.doi.org/10.1002/9781118785706.ch15.

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da Rocha, Eliana Maria Mauricio, Gilberto Fontes, and John Patrick Ehrenberg. "Lymphatic Filariasis." In Arthropod Borne Diseases, 369–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-13884-8_24.

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Földi, Etelka. "Lymphatic Vascular Diseases." In Pan Vascular Medicine, 1538–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56225-9_96.

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Graves, Patricia M., Peter Wood, and Hervé C. Bossin. "Lymphatic Filariasis in Oceania." In Neglected Tropical Diseases, 101–42. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43148-2_4.

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Sodahlon, Yao, Mwele Malecela, and John O. Gyapong. "Lymphatic Filariasis (Elephantiasis)." In Neglected Tropical Diseases - Sub-Saharan Africa, 159–86. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25471-5_8.

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Daróczy, Judit. "Lymphovascular Alterations in Selected Dermatological Diseases." In The Dermal Lymphatic Capillaries, 137–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73480-9_20.

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Rajamanickam, Anuradha, and Subash Babu. "Overview on Lymphatic Filariasis in South Asia." In Neglected Tropical Diseases, 137–69. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-68493-2_5.

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Tang, Min, Hui Dai, Heng Liu, Yang Cao, Shuang Xia, and Ying Zou. "Lymphatic Gland Lesions in Neck." In Radiology of Infectious and Inflammatory Diseases - Volume 2, 349–57. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8841-6_31.

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Despommier, Dickson D., Robert W. Gwadz, and Peter J. Hotez. "Lymphatic Filariae: Wuchereria bancrofti (Cobbold 1877) and Brugia malayi (Brug 1927)." In Parasitic Diseases, 40–47. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4612-2476-1_7.

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Soni, Mukesh, Mayank Handa, and Rahul Shukla. "Nano Drug Delivery Approaches for Lymphatic Filariasis Therapeutics." In Nanotechnology for Infectious Diseases, 263–79. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-9190-4_12.

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Conference papers on the topic "Hemic and Lymphatic Diseases"

1

Elshazly, Hanaa, Ahmed Taher Azar, Abeer El-korany, and Aboul Ella Hassanien. "Hybrid system for lymphatic diseases diagnosis." In 2013 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2013. http://dx.doi.org/10.1109/icacci.2013.6637195.

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Baati, Karim, Tarek M. Hamdani, and Adel M. Alimi. "Diagnosis of Lymphatic Diseases Using a Naive Bayes Style Possibilistic Classifier." In 2013 IEEE International Conference on Systems, Man and Cybernetics (SMC 2013). IEEE, 2013. http://dx.doi.org/10.1109/smc.2013.772.

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Norlia, A. "Lymphatic mapping and sentinel lymph node biopsy in patients with invasive breast cancer: The UKM experience." In Asian Breast Diseases Association (ABDA) 3rd Teaching Course: Advances in the Management of Breast Diseases. Kuantan, Malaysia: Asian Breast Diseases Association, 2005. http://dx.doi.org/10.2349/biij.1.1.e6-22.

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Weiler, Michael, and J. Brandon Dixon. "Characterization of Near-Infrared Functional Lymphatic Imaging in the Rat Tail Model." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14765.

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The lymphatic vasculature is present in nearly every tissue of the body to serve essential functions in fluid homeostasis, immune cell trafficking, and lipid transport, and it has been implicated in the progression of several diseases. Despite the critical roles that this system performs, very little is known about the lymphatic vasculature in comparison to the blood vasculature, which can be attributed, in part, to the difficulty associated with imaging lymphatic vessels. With the growing interest in studying lymphatics, near-infrared (NIR) imaging has emerged in the literature as a novel lymphatic imaging modality to simultaneously improve spatial resolution to visualize small initial lymphatics and increase temporal resolution to capture the dynamic lymphatic pump function responsible for fluid propulsion.
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Simonova, MV, VI Vasiliev, and NS Shornikova. "AB0121 Cytostatics effect on the development of malignant and lymphatic proliferative formations during sjorgen?s disease (ss)." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.304.

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Faulkner, M. F., and J. Brandon Dixon. "Engineered Model of the Intestine Suggests Active Transport of Lipid by Lymphatics." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53903.

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The lymphatic system has long been thought of as little more than a series of passive ducts as they serve to return fluid and proteins from interstitial spaces back to the blood, provide a route for immune cell trafficking, and transport dietary lipid from the intestine to the blood. Recent evidence has revealed that the lymphatics play an active role in lipid trafficking, and alterations in this function have been correlated with the presence of lymphatic diseases (Dixon, 2010). Here we describe the use of a two-cell, tissue engineered model to explore mechanisms of lipid transport across lymphatic endothelial cells (LEC). Previously this model was demonstrated to recapitulate essential features of the intestinal-lacteal interface with in the mammalian gut (Dixon et al., 2009). With our model we demonstrate, not only that lipid transport across the lymphatics is transcellular and ATP dependent, but also, this mechanism of transport utilizes the molecular motors dynein and kinesin.
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CIURBA PASTOR, Anca-Paula, Ionel HAIDU, Ovidiu GACEU, and Mihaela BIRIȘ MATEI. "The Thermal Water in Bihor County and its Benefits for Treating Arthritis. A Case Study: Băile 1 Mai Resort." In Air and Water – Components of the Environment 2022 Conference Proceedings. Casa Cărţii de Ştiinţă, 2022. http://dx.doi.org/10.24193/awc2022_21.

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Due to the existence of important thermal water resources, in Bihor County there are many locations where thermo-mineral waters are used for bathing or for leisure. In this study, we focus on the spas in Bihor County (Băile Felix, Băile 1 Mai, Băile Tinca, Stâna de Vale, to which we add the village of Sarcău), where these waters have been used for a long time and which have the necessary infrastructure for therapy. Thus, we aim to highlight the particularities of these waters, the presentation of the balneotherapy procedures used and the emphasis on the beneficial effects of balneotherapy on osteoarthritis (most of the pathologies treated here are osteoarthritis). In the spa treatment bases, along with thermal water, other procedures are used that enhance the effect of these waters (physiotherapy, TENS (transcutaneous electrical nerve stimulation), TCARE (capacitive and resistive electrical transfer), therapeutic massage, lymphatic drainage massage, ultrasound, electrotherapy, low frequency electromagnetic pulse therapy, galvanic baths, paraffin wraps, laser therapy). The main pathologies treated by the mentioned procedures are inflammatory rheumatic diseases, neuromuscular diseases.
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