77 research outputs found
MSS D Multispectral Scanner System
The development and acceptance testing of the 4-band Multispectral Scanners to be flown on LANDSAT D and LANDSAT D Earth resources satellites are summarized. Emphasis is placed on the acceptance test phase of the program. Test history and acceptance test algorithms are discussed. Trend data of all the key performance parameters are included and discussed separately for each of the two multispectral scanner instruments. Anomalies encountered and their resolutions are included
Hepatitis B virus-infection related cryoglobulinemic vasculitis. Clinical manifestations and the effect of antiviral therapy: A review of the literature
Objective: Hepatitis B virus (HBV) infection causes chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Furthermore, about 20% of the patients develop extrahepatic manifestations such as cryoglobulinemic vasculitis (CV), polyarteritis nodosa, non-rheumatoid arthritis, glomerulonephritis and non-Hodgkin lymphoma. This review analyzed literature data on clinical manifestations of HBV-related CV and the impact of antiviral therapy with analoques nucleotide. Methods: A PubMed search was performed to select eligible studies in the literature, up to July 2022. Results: Some studies have analyzed clinical manifestations in HBV-related CV and have investigated the role of antiviral therapy with nucleotides analogues (NAs). Clinical manifestations of CV vary from mild to moderate (purpura, asthenia and arthralgias) to severe (leg ulcers, peripheral neuropathy, glomerulonephritis, and non-Hodking lymphoma). NAs therapy leads to suppression of HBV-DNA; therefore, it is capable of producing clinical response in the majority of patients with mild to moderate symptoms. Conclusion: Antiviral therapy with NAs is the first choice for HBV suppression and control of mild to moderate disease. In severe vasculitis (glomerulonephritis, progressive peripheral neuropathy and leg ulcers), rituximab alone or with plasma-exchange is always indicated in combination with antiviral therapy
Management of mixed cryoglobulinemia with rituximab: evidence and consensus-based recommendations from the Italian Study Group of Cryoglobulinemia (GISC)
Cryoglobulinemic vasculitis (CV) or mixed cryoglobulinemic syndrome (MCS) is a systemic small-vessel vasculitis characterized by the proliferation of B-cell clones producing pathogenic immune complexes, called cryoglobulins. It is often secondary to hepatitis C virus (HCV), autoimmune diseases, and hematological malignancies. CV usually has a mild benign clinical course, but severe organ damage and life-threatening manifestations can occur. Recently, evidence in favor of rituximab (RTX), an anti-CD 20 monoclonal antibody, is emerging in CV: nevertheless, questions upon the safety of this therapeutic approach, especially in HCV patients, are still being issued and universally accepted recommendations that can help physicians in MCS treatment are lacking. A Consensus Committee provided a prioritized list of research questions to perform a systematic literature review (SLR). A search was made in Medline, Embase, and Cochrane library, updated to August 2021. Of 1227 article abstracts evaluated, 27 studies were included in the SLR, of which one SLR, 4 RCTs, and 22 observational studies. Seventeen recommendations for the management of mixed cryoglobulinemia with rituximab from the Italian Study Group of Cryoglobulinemia (GISC) were developed to give a valuable tool to the physician approaching RTX treatment in CV
Abnormal CD4 + T helper (Th) 1 cells and activated memory B cells are associated with type III asymptomatic mixed cryoglobulinemia in HCV infection
The preparation of thoria
http://www.archive.org/details/preparationoftho00wilsThesis (B.S.)--Armour Institute of Technolog
Hepatitis C virus infection and mixed cryoglobulinemia
Hepatitis C virus (HCV) chronic infection is recognized as the major cause of mixed cryoglobulinemia (MC). Its persistence
represents a continuous stimulus for host immune system with production of circulating immune complexes (ICs), one-third of
them with cryoprecipitate property. Several factors contribute to the biological activities of ICs, many of which are not completely
known. Among them, complement factors play a crucial role in the cold-insoluble ICs-mediated vasculitis, involving primarily
small blood vessels in different tissues including skin, kidney, peripheral, and central nervous system. Liver represents the major
target of HCV infection with inflammatory infiltrates, resembling secondary lymphoid follicles. Cytokine like CXCL13 contribute
to B-cell homing in intraportal lymphoid aggregates, in which B-cell clonal selection may arise. B-cell clonal expansion starts
as an antigen-driven event and expands towards indolent and malignant B-cell proliferation. Occurrence of intrahepatic Bcell
clonalities correlates with extrahepatic clinical manifestations of HCV infection. In this context, cryoglobulinemic patients
should be considered a peculiar HCV-infected population that needs a clinical multidisciplinary approach and more articulated
therapeutic measures
IN SITU SIMULTANEOUS DETECTION OF HEPATITIS C VIRUS RNA AND HEPATITIS C VIRUS-RELATED ANTIGENS IN HEPATOCELLULAR CARCINOMA
Background: The overwhelming evidence that chronic infection with the hepatitis C virus (HCV) is an important cause of hepatocellular carcinoma (HCC) is based on epidemiologic, casecontrol, and cohort studies as well as laboratory investigations. To address better the pathogenesis of HCV infection at a single cell level, the authors developed a specific reproducible method for the simultaneous detection of HCV specific sequences and antigens in liver tissue, using a combination of nonradioactive in situ hybridization and immunohistochemistry. Methods: After immunoistochemical staining of the liver sections for E2/NS-1, C22–3, C33c, C100–3 and NS-5 antigens with immunogold-silver technique, in situ hybridization was performed on the same sections using digoxigenin-labeled HCV 5 NonCoding
specific probes. The hybridization signal was detected by an antidigoxigenin, Fab fragment-alkaline phosphatase conjugate. This simultaneous detection permitted the subcellular localization of HCV RNA and antigens with excellent preservation of tissue morphology and absence of background staining. In addition the types and percentages of cells harboring HCV in tissue could be determined. Results: The in situ detection of HCV showed positive signals in both cancerous and noncancerous areas of liver tissue in six of six HCV-infected patients with HCC and in none of four controls, including three HCV negative HCC patients and one patient with epithelioid hemangioendothelioma. Two classes of infected cells were distinguished throughout the liver: (1) cells containing large amounts of negative-stranded HCV RNA, which were probably undergoing active viral replication; and (2) cells displaying positive-stranded HCV RNA only, with unpredictable levels of viral replication. Both types expressed core, envelope, and NS-3, -4, -5 proteins. HCV RNA and antigens were exclusively cytoplasmic. Detection of viral proteins was highly predictive of the presence of large amounts of HCV RNA in the same cell. Fewer HCV positive cells were consistently demonstrated in the cancerous area. Conclusions: These findings support the contention that HCVinfects hepatocytes and replicates in them, even after their malignant transformation
Trattamento antivirale in pazienti affetti da epatite cronica attiva HCV correlata e transaminasi normali
B CELLS AND HCV: AN INFECTION MODEL OF AUTOIMMUNITY
In addition to cause acute and chronic liver disease, hepatitis C virus (HCV) infection is frequently associated to autoimmune disorders, such as mixed cryoglobulinemia, primary glomerulonephritis, monoclonal gammopathy of undetermined significance and post-transplant proliferative disorders. Progression to malignant phenotype of B cells may be the consequence of additional genetic events or abnormal conditions resulting from modification of host cell genes involved in the control of oncogenes and oncoproteins. In this review, we will address the potential immune disregulatory mechanism(s) underlying HCV persistence. In addition, HCV/B-cell interaction that might explain defects in humoral immunity in individuals who develop chronic virus carriage and lymphoproliferative disorders will be emphasized
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