Publications by authors named "Christine Korteweg"

Article Synopsis
  • * The study analyzed 1,070 patients with respiratory symptoms at six medical centers, comparing chest CT results to RT-PCR tests and a clinical reference standard established by a group of medical professionals.
  • * Chest CT demonstrated strong diagnostic performance, with an area under the curve (AUC) of 0.87 for both RT-PCR and clinical reference standards, indicating that higher CO-RADS scores significantly correlated with the likelihood of a COVID-19 diagnosis.
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Cystic or cavitating lung nodules may reflect an additional diagnostic challenge in benign metastasizing leiomyoma. Our case underlines the importance of combining clinical and radiological findings with specific pulmonary pathology consultation.

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CF is caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) which is an anion selective transmembrane ion channel that mainly regulates chloride transport, expressed in the epithelia of various organs. Recently, we have demonstrated CFTR expression in the brain, the spinal cord and the sympathetic ganglia. This study aims to investigate the expression and distribution of CFTR in the ganglia of the human gastrointestinal tract.

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Study Question: How does the placenta protect the fetus from immune rejection by the mother?

Summary Answer: The placenta can produce IgG that is glycosylated at one of its Fab arms (asymmetric IgG; aIgG) which can interact with other antibodies and certain leukocytes to affect local immune reactions at the junction between the two genetically distinct entities.

What Is Known Already: The placenta can protect the semi-allogenic fetus from immune rejection by the immune potent mother. aIgG in serum is increased during pregnancy and returns to the normal range after giving birth.

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The placenta is known to protect the fetus from infection and maternal rejection. In a previous study, we demonstrated that placental trophoblasts can synthesize immunoglobulin G (IgG). In this study, we investigated the distribution of immunoglobulins (IgG, IgM, and IgA), IgG receptors (FcRn and FcgammaRIII), and complement proteins in placental trophoblasts at the ultrastructural level.

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The liver has the extraordinary properties of regeneration and immune tolerance; however, the mechanisms governing these abilities are poorly understood. To address these questions, we examined the possible expression of immunoglobulins in the human and rat liver and the relationship of IgG expression to hepatocyte proliferation, metastasis, apoptosis and immune tolerance. Immunohistochemistry, in situ hybridization, laser-guided microdissection and reverse transcription-PCR were performed to examine the expression of IgG in normal human and rat liver, severe combined immunodeficient mouse (SCID) liver and human liver cancers and corresponding cell lines.

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Introduction: Recently, growing evidence indicates that immunoglobulins (Igs) are not only produced by mature B lymphocytes or plasma cells, but also by various normal cells types at immune privileged sites and neoplasm, including breast cancer. However, the association of breast cancer derived IgG with genesis and development of the disease has not yet been established.

Methods: In this study we examined the expression of IgG in 186 breast cancers, 20 benign breast lesions and 30 normal breast tissues.

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Increasing evidence indicates that various cancer cell types are capable of producing IgG. The exact function of cancer-derived IgG has, however, not been elucidated. Here we demonstrated the expression of IgG genes with V(D)J recombination in 80 cases of colorectal cancers, 4 colon cancer cell lines and a tumor bearing immune deficient mouse model.

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Background: In spite of recent advances in treatment strategies, prostate cancer (PCa) remains the second leading cause of cancer death in men with its genetic and biologic behaviors still poorly understood. Recently, accumulating evidence indicates that cancer cells, as well as some normal cells can secret IgG. This study was designed to evaluate IgG gene expression and its possible significance in PCa tissue samples and cell lines.

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Except for the well-known immunoglobulin G (IgG) producing cell types, ie, mature B lymphocytes and plasma cells, various non-lymphoid cell types, including human cancer cells, neurons, and some specified epithelial cells, have been found to express IgG. In this study, we detected the expression of the heavy chain of IgG (IgGγ) and kappa light chain (Igκ) in papillary thyroid cancer cells. Using in situ hybridization, we detected the constant region of human IgG1 (IGHG1) in papillary thyroid cancer cells.

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We and other research groups have previously shown that various cancer types can express immunoglobulin G, but investigation on of immunoglobulin G expression in esophageal cancer, a highly malignant tumor, and its biological significance has been lacking. In this study, we examined immunoglobulin G protein and its messenger RNA, as well as the expressions of recombination-activating gene 1, recombination-activating gene 2, and activation-induced cytidine deaminase in 142 cases of esophageal cancer tissues, and 2 esophageal cancer cell lines (Eca109, SHEEC). We also compared their expressions with tumor grade and a proliferation marker, Ki67.

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Recently immunoglobulins (Igs) have been found to be expressed by cells other than B lymphocytes, including various human carcinoma cells. Sarcomas are derived from mesenchyme, and the knowledge about the occurrence of Ig production in sarcoma cells is very limited. Here we investigated the phenomenon of immunoglobulin G (IgG) expression and its molecular basis in 3 sarcoma cell lines.

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It has long been accepted that immunoglobulins (Igs) were produced by B lymphoid cells only. Recently Igs have been found to be expressed in various human cancer cells and promote tumor growth. Recombination activating gene 1 (RAG1) and RAG2, which are essential enzymes for initiating variable-diversity-joining segment recombination, have also been found to be expressed in cancer cells.

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Traditional views hold that immunoglobulin G (IgG) in the human umbilical cord is internalized by human umbilical endothelial cells for passive immunity. In this study, the protein and mRNA transcripts of IgG were found in the cytoplasm of human umbilical endothelial cells by immunohistochemistry, in situ hybridization, and reverse transcription PCR (RT-PCR). The essential enzymes for IgG synthesis and assembling, RAG1 (recombination activating gene 1), RAG2, and variable (V), diversity (D), and joining (J) segments for recombination of IgG, were also found in these cells by RT-PCR and real-time PCR.

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Recently, accumulating evidence has shown that several immunological molecules previously thought to be exclusively expressed by immune cells are also produced by nervous cells. Such molecules are thought to participate in the cross-talk between the immune and the nervous systems. IgG, an important immunological molecule, was traditionally thought to be produced by B lymphocytes only.

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It has recently been demonstrated that not only mature B lymphocytes, but also non-lymphoid cells, including cancer cells and neurons, express IgG. In the eye, an important immune privileged site, the presence of IgG has been ascribed to IgG entering the eye through breaches of the blood–ocular barrier. Here we demonstrate that the eye itself can produce IgG intrinsically.

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The cystic fibrosis transmembrane conductance regulator (CFTR) is an important protein that acts as a chloride channel and regulates many physiological functions, including salt transport and fluid flow. Mutations in the gene encoding the CFTR protein cause cystic fibrosis. CFTR is expressed in the epithelial cells of the lungs, pancreas, intestines, and other organs.

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It is known that severe acute respiratory syndrome (SARS), a severe infectious illness, which caused an epidemic in Asia in 2003, has extensive and complex effects on human organ systems. It has been reported that the serum levels of prolactin (PRL), follicle stimulating hormone (FSH), and luteinizing hormone (LH) of SARS patients are significantly higher than those of control groups, while estradiol (E2), pregnancy hormone (P), and thyroid stimulating hormone (TSH) are considerably lower than those of normal controls. This phenomenon suggests that the adenohypophyseal endocrine cells in SARS patients may be damaged.

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The 2009 H1N1 and H5N1 influenza viruses are newly (re-) emerged influenza A viruses (2009 A(H1N1) and A(H5N1), respectively) that have recently posed tremendous health threats in many regions worldwide. With the 2009 outbreak of H1N1 influenza A, the world witnessed the first influenza pandemic of the 21st century. The disease has rapidly spread across the entire globe, and has resulted in hundreds of thousands of cases with confirmed infection.

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H5N1 avian influenza is a highly fatal infectious disease that could cause a potentially devastating pandemic if the H5N1 virus mutates into a form that spreads efficiently among humans. Recent findings have led to a basic understanding of cell and organ histopathology caused by the H5N1 virus. Here we review the pathology of H5N1 avian influenza reported in postmortem and clinical studies and discuss the key pathogenetic mechanisms.

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Avian and human influenza viruses preferentially bind to alpha-2,3-linked and alpha-2,6-linked sialic acids, respectively. Until today, the distributions of these two receptor types had never been investigated in H5N1-infected human tissue samples. Here, the expression of avian (AIV-Rs) and human influenza receptors (HuIV-Rs) is studied in various organs (upper and lower respiratory tracts, brain, placenta, liver, kidney, heart, intestines, and spleen) of two H5N1 cases and 14 control cases.

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Background: Human infection with avian influenza H5N1 is an emerging infectious disease characterised by respiratory symptoms and a high fatality rate. Previous studies have shown that the human infection with avian influenza H5N1 could also target organs apart from the lungs.

Methods: We studied post-mortem tissues of two adults (one man and one pregnant woman) infected with H5N1 influenza virus, and a fetus carried by the woman.

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Severe acute respiratory syndrome (SARS) is an acute respiratory disease with significant morbidity and mortality. While its clinical manifestations have been extensively studied, its pathogenesis is not yet fully understood. A limited number of autopsy studies have revealed that the lungs and the immune system are the organs that sustain the most severe damage.

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Severe acute respiratory syndrome (SARS) is an emerging infectious viral disease characterized by severe clinical manifestations of the lower respiratory tract. The pathogenesis of SARS is highly complex, with multiple factors leading to severe injury in the lungs and dissemination of the virus to several other organs. The SARS coronavirus targets the epithelial cells of the respiratory tract, resulting in diffuse alveolar damage.

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Severe acute respiratory syndrome (SARS) is a novel infectious disease with disastrous clinical consequences, in which the lungs are the major target organs. Previous studies have described the general pathology in the lungs of SARS patients and have identified some of the cell types infected by SARS coronavirus (SARS-CoV). However, at the time of this writing, there were no comprehensive reports of the cellular distribution of the virus in lung tissue.

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