The Experts below are selected from a list of 123 Experts worldwide ranked by ideXlab platform
James T Harvey - One of the best experts on this subject based on the ideXlab platform.
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ANTIBODIES TO PHOCINE HERPESVIRUS-1 ARE COMMON IN NORTH AMERICAN HARBOR SEALS (PHOCA VITULINA)
Journal of Wildlife Diseases, 2003Co-Authors: Tracey Goldstein, Frances M D Gulland, James T Harvey, Brian Michael Aldridge, Teri Rowles, Dyanna M. Lambourn, Steven J. Jeffries, Lena N. Measures, Pamela K. Yochem, Brent S. StewartAbstract:Phocine herpesvirus-1 (PhHV-1) has been associated with morbidity and high mortality in neonatal harbor seals (Phoca vitulina) along the Pacific coast of California (USA) and in northern Europe. Seals dying with PhHV-1 associated disease in California primarily have histopathologic evidence of Adrenal Necrosis or Adrenalitis with herpesviral inclusion bodies. Little is known about prevalence of exposure to PhHV-1, modes of disease transmission, and viral pathogenesis in free-ranging harbor seal populations. To evaluate the prevalence in North America, 866 serum samples collected between 1994 and 2002 from harbor seals captured or stranded on the Pacific and Atlantic coasts of North America were assayed by enzyme linked immunosorbent assay (ELISA) for evidence of PhHV-1 exposure. Samples from three harbor seal age classes (pre-weaned, weaned, and subadults/adults) were obtained from each of four regions to compare exposure among sex, age class, and region. We found increasing prevalence with age as 37.5% o...
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Adrenal function in wild and rehabilitated pacific harbor seals phoca vitulina richardii and in seals with phocine herpesvirus associated Adrenal Necrosis
Marine Mammal Science, 1999Co-Authors: Frances M D Gulland, Martin Haulena, Linda J Lowenstine, C Munro, Peter A Graham, J Bauman, James T HarveyAbstract:Adrenal function in harbor seals (Phoca vitulina richardii) was evaluated using adrenocorticotrophic hormone (ACTH) stimulation tests and fecal cortisol levels. The effect of ACTH administration on plasma cortisol and aldosterone levels in five free-living and 14 rehabilitated harbor seal pups was determined using enzyme immunoassay and radioimmunoassay, respectively. In free-living seals, injection of ACTH caused a significant increase in mean plasma cortisol but not of mean aldosterone levels 60 min postinjection. In these seals, mean initial plasma aldosterone was significantly higher than initial levels in rehabilitated seals, while initial cortisol levels were similar. Of the rehabilitated seals, eight died with Adrenal cortical Necrosis associated with herpesvirus inclusions, while six lived to be released. In the seals that were released, both mean initial cortisol levels and response to ACTH decreased through rehabilitation. In the seals that died, mean initial cortisol and response to ACTH increased through rehabilitation. The differences between initial cortisol levels in seals that lived and those that died were significant at weeks two and four of rehabilitation but not at the week of admission. There was considerable individual variation in initial plasma aldosterone levels and responses to ACTH, although initial aldosterone levels were significantly higher in rehabilitated seals that died than in seals that lived. Seals with Adrenal Necrosis associated with herpesvirus infection did not have decreased Adrenal hormone responses to ACTH. Differences between initial hormone levels and responses to ACTH in different groups of seals may be associated with differing stress levels. Fecal cortisol assays were not a useful method of assessing Adrenal function in these seals, as measured levels did not correlate with plasma cortisol levels.
Kaoru Nagata - One of the best experts on this subject based on the ideXlab platform.
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the first case of thrombocytopenia anasarca fever renal impairment or reticulin fibrosis and organomegaly tafro syndrome with unilateral Adrenal Necrosis a case report
Journal of Medical Case Reports, 2018Co-Authors: Yu Fujiwara, Akito Takamura, Kaoru NagataAbstract:TAFRO syndrome, which was first reported in 2010 in Japan, is a relatively rare disease characterized by thrombocytopenia, anasarca, fever, renal impairment, reticulin fibrosis, and organomegaly. Although this disease is considered similar to multicentric Castleman disease, some of the clinical features, such as thrombocytopenia, are different from typical cases of multicentric Castleman disease. In addition, the etiology of TAFRO syndrome remains unknown and controversial. There have only been a few cases of TAFRO syndrome complicated with Adrenal gland lesions, and all of them have had hemorrhagic involvement. This report describes the case of a 46-year-old Asian man who presented with fever, epigastric pain, and back pain for 1 month. A computed tomographic scan revealed ascites, mild lymphadenopathy, and left Adrenal Necrosis without hemorrhage. A blood test showed thrombocytopenia, anemia, and elevated C-reactive protein, alkaline phosphatase, and creatinine levels. Based on the edema, severe thrombocytopenia, fever, reticulin myelofibrosis shown by bone marrow biopsy, mild lymphadenopathy, and progressive renal insufficiency, we diagnosed this patient as having TAFRO syndrome. He was successfully treated by immediate administration of glucocorticoids and tocilizumab. There have been no previous reports of a case of TAFRO syndrome complicated with Adrenal Necrosis. Because the biopsy of the left Adrenal gland revealed Necrosis without any evidence of hemorrhage, we concluded that the unilateral Adrenal Necrosis in this case was caused by either ischemia from infarction or organomegaly itself under severe hypercytokinemia. This unusual clinical course is useful for further analysis of the etiology of TAFRO syndrome.
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The first case of thrombocytopenia, anasarca, fever, renal impairment or reticulin fibrosis, and organomegaly (TAFRO) syndrome with unilateral Adrenal Necrosis: a case report
Journal of Medical Case Reports, 2018Co-Authors: Yu Fujiwara, Akito Takamura, Kaoru NagataAbstract:Background TAFRO syndrome, which was first reported in 2010 in Japan, is a relatively rare disease characterized by thrombocytopenia, anasarca, fever, renal impairment, reticulin fibrosis, and organomegaly. Although this disease is considered similar to multicentric Castleman disease, some of the clinical features, such as thrombocytopenia, are different from typical cases of multicentric Castleman disease. In addition, the etiology of TAFRO syndrome remains unknown and controversial. There have only been a few cases of TAFRO syndrome complicated with Adrenal gland lesions, and all of them have had hemorrhagic involvement. Case presentation This report describes the case of a 46-year-old Asian man who presented with fever, epigastric pain, and back pain for 1 month. A computed tomographic scan revealed ascites, mild lymphadenopathy, and left Adrenal Necrosis without hemorrhage. A blood test showed thrombocytopenia, anemia, and elevated C-reactive protein, alkaline phosphatase, and creatinine levels. Based on the edema, severe thrombocytopenia, fever, reticulin myelofibrosis shown by bone marrow biopsy, mild lymphadenopathy, and progressive renal insufficiency, we diagnosed this patient as having TAFRO syndrome. He was successfully treated by immediate administration of glucocorticoids and tocilizumab. Conclusions There have been no previous reports of a case of TAFRO syndrome complicated with Adrenal Necrosis. Because the biopsy of the left Adrenal gland revealed Necrosis without any evidence of hemorrhage, we concluded that the unilateral Adrenal Necrosis in this case was caused by either ischemia from infarction or organomegaly itself under severe hypercytokinemia. This unusual clinical course is useful for further analysis of the etiology of TAFRO syndrome.
Frances M D Gulland - One of the best experts on this subject based on the ideXlab platform.
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ANTIBODIES TO PHOCINE HERPESVIRUS-1 ARE COMMON IN NORTH AMERICAN HARBOR SEALS (PHOCA VITULINA)
Journal of Wildlife Diseases, 2003Co-Authors: Tracey Goldstein, Frances M D Gulland, James T Harvey, Brian Michael Aldridge, Teri Rowles, Dyanna M. Lambourn, Steven J. Jeffries, Lena N. Measures, Pamela K. Yochem, Brent S. StewartAbstract:Phocine herpesvirus-1 (PhHV-1) has been associated with morbidity and high mortality in neonatal harbor seals (Phoca vitulina) along the Pacific coast of California (USA) and in northern Europe. Seals dying with PhHV-1 associated disease in California primarily have histopathologic evidence of Adrenal Necrosis or Adrenalitis with herpesviral inclusion bodies. Little is known about prevalence of exposure to PhHV-1, modes of disease transmission, and viral pathogenesis in free-ranging harbor seal populations. To evaluate the prevalence in North America, 866 serum samples collected between 1994 and 2002 from harbor seals captured or stranded on the Pacific and Atlantic coasts of North America were assayed by enzyme linked immunosorbent assay (ELISA) for evidence of PhHV-1 exposure. Samples from three harbor seal age classes (pre-weaned, weaned, and subadults/adults) were obtained from each of four regions to compare exposure among sex, age class, and region. We found increasing prevalence with age as 37.5% o...
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Adrenal function in wild and rehabilitated pacific harbor seals phoca vitulina richardii and in seals with phocine herpesvirus associated Adrenal Necrosis
Marine Mammal Science, 1999Co-Authors: Frances M D Gulland, Martin Haulena, Linda J Lowenstine, C Munro, Peter A Graham, J Bauman, James T HarveyAbstract:Adrenal function in harbor seals (Phoca vitulina richardii) was evaluated using adrenocorticotrophic hormone (ACTH) stimulation tests and fecal cortisol levels. The effect of ACTH administration on plasma cortisol and aldosterone levels in five free-living and 14 rehabilitated harbor seal pups was determined using enzyme immunoassay and radioimmunoassay, respectively. In free-living seals, injection of ACTH caused a significant increase in mean plasma cortisol but not of mean aldosterone levels 60 min postinjection. In these seals, mean initial plasma aldosterone was significantly higher than initial levels in rehabilitated seals, while initial cortisol levels were similar. Of the rehabilitated seals, eight died with Adrenal cortical Necrosis associated with herpesvirus inclusions, while six lived to be released. In the seals that were released, both mean initial cortisol levels and response to ACTH decreased through rehabilitation. In the seals that died, mean initial cortisol and response to ACTH increased through rehabilitation. The differences between initial cortisol levels in seals that lived and those that died were significant at weeks two and four of rehabilitation but not at the week of admission. There was considerable individual variation in initial plasma aldosterone levels and responses to ACTH, although initial aldosterone levels were significantly higher in rehabilitated seals that died than in seals that lived. Seals with Adrenal Necrosis associated with herpesvirus infection did not have decreased Adrenal hormone responses to ACTH. Differences between initial hormone levels and responses to ACTH in different groups of seals may be associated with differing stress levels. Fecal cortisol assays were not a useful method of assessing Adrenal function in these seals, as measured levels did not correlate with plasma cortisol levels.
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HERPESVIRUS INFECTION IN STRANDED PACIFIC HARBOR SEALS OF COASTAL CALIFORNIA
Journal of Wildlife Diseases, 1997Co-Authors: Frances M D Gulland, Linda J Lowenstine, Jean-martin Lapointe, Terry R. Spraker, Donald P. KingAbstract:Histopathological examination revealed multifocal acute to chronic Adrenal Necrosis in 74 of 162 (45%) Pacific harbor seal pups (Phoca vitulina richardsi) dying during rehabilitation following live stranding along the coast of central and northern California (USA). Necrotic Adrenal cells contained amphophilic, smudgy intranuclear inclusion bodies that were stained positive for DNA. Fifty of these seals also had lesions typical of sepsis, bacterial omphalophlebitis, pneumonia or gastroenteritis. Twenty four seals had no lesions other than thymic atrophy and occasional multifocal hepatic Necrosis. Prior to death, affected seals had a marked lymphopenia. Electron microscopy revealed unenveloped intranuclear hexagonal to round viral particles approximately 100 nm in diameter, and cytoplasmic enveloped virions approximately 160 nm in diameter. These were morphologically consistent with herpesvirus. Inoculation of phocine Adrenal and kidney cell lines with an Adrenal tissue homogenate from affected animals prod...
Robert Salvayre - One of the best experts on this subject based on the ideXlab platform.
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new pathogenetic hypothesis for wolman disease possible role of oxidized low density lipoproteins in Adrenal Necrosis and calcification
Biochemical Journal, 1994Co-Authors: G Fitoussi, Anne Negresalvayre, Marietherese Pieraggi, Robert SalvayreAbstract:Wolman disease in an inherited metabolic disease, characterized by a severe deficiency of the acid lipase and a massive lysosomal storage of triacylglycerols and cholesteryl esters, associated with hepatosplenomegaly, Adrenal calcification and nearly always fatal in the first year of life. Cultured human lymphoblastoid cells and human Adrenal cells are able to promote the formation of mildly oxidized low-density lipoproteins (LDL), which in turn exhibit a non-negligible cytotoxic effect on these cells. In contrast, fibroblasts induce only very low levels of LDL oxidation. Comparative experiments have shown that the cytotoxic effect of oxidized LDL was higher to Wolman-disease cells than to controls. The oxidative ability of Wolman cells was similar to that of normal ones. The over-cytotoxicity of mildly oxidized LDL to Wolman cells resulted from the higher uptake of mildly oxidized LDL through the LDL-receptor pathway, which is only poorly down-regulated in Wolman cells subsequently to the block of the lysosomal degradation of LDL-cholesteryl esters. In cultured Adrenal cells, oxidized LDL induced a sustained rise in intracellular [Ca2+] which is directly involved in the cellular damage and cell death induced by oxidized LDL [Negre-Salvayre and Salvayre (1992) Biochim. Biophys. Acta 1123, 207-215]. This Ca2+ peak is followed by a dramatic deposition of calcium in damaged or/and dead cultured Adrenal cells, quite similar to that observed in Wolman-disease Adrenal cortex. The cell-induced LDL oxidation and the subsequent cytotoxic effect can be prevented, at least in part, by antioxidants such as alpha-tocopherol and nordihydroguaiaretic acid. These findings support the hypothesis that the Wolman-disease Adrenal damage (Necrosis and calcification) could result from the association of the following events: mild oxidation of LDL by Adrenal cells, over-uptake of mildly oxidized LDL by Wolman cells (resulting from the block of the lysosomal degradation of cholesteryl esters in Wolman cells), and cytotoxicity related to the amount of mildly oxidized LDL internalized by cells. The reported data also suggest that LDL oxidation induced by Adrenal cells and their subsequent cytotoxicity can be prevented (in part) by antioxidants, and the potential therapeutic use of antioxidants in Wolman disease is discussed.
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New pathogenetic hypothesis for Wolman disease: possible role of oxidized low-density lipoproteins in Adrenal Necrosis and calcification.
The Biochemical journal, 1994Co-Authors: G Fitoussi, Marietherese Pieraggi, A Nègre-salvayre, Robert SalvayreAbstract:Wolman disease in an inherited metabolic disease, characterized by a severe deficiency of the acid lipase and a massive lysosomal storage of triacylglycerols and cholesteryl esters, associated with hepatosplenomegaly, Adrenal calcification and nearly always fatal in the first year of life. Cultured human lymphoblastoid cells and human Adrenal cells are able to promote the formation of mildly oxidized low-density lipoproteins (LDL), which in turn exhibit a non-negligible cytotoxic effect on these cells. In contrast, fibroblasts induce only very low levels of LDL oxidation. Comparative experiments have shown that the cytotoxic effect of oxidized LDL was higher to Wolman-disease cells than to controls. The oxidative ability of Wolman cells was similar to that of normal ones. The over-cytotoxicity of mildly oxidized LDL to Wolman cells resulted from the higher uptake of mildly oxidized LDL through the LDL-receptor pathway, which is only poorly down-regulated in Wolman cells subsequently to the block of the lysosomal degradation of LDL-cholesteryl esters. In cultured Adrenal cells, oxidized LDL induced a sustained rise in intracellular [Ca2+] which is directly involved in the cellular damage and cell death induced by oxidized LDL [Nègre-Salvayre and Salvayre (1992) Biochim. Biophys. Acta 1123, 207-215]. This Ca2+ peak is followed by a dramatic deposition of calcium in damaged or/and dead cultured Adrenal cells, quite similar to that observed in Wolman-disease Adrenal cortex. The cell-induced LDL oxidation and the subsequent cytotoxic effect can be prevented, at least in part, by antioxidants such as alpha-tocopherol and nordihydroguaiaretic acid. These findings support the hypothesis that the Wolman-disease Adrenal damage (Necrosis and calcification) could result from the association of the following events: mild oxidation of LDL by Adrenal cells, over-uptake of mildly oxidized LDL by Wolman cells (resulting from the block of the lysosomal degradation of cholesteryl esters in Wolman cells), and cytotoxicity related to the amount of mildly oxidized LDL internalized by cells. The reported data also suggest that LDL oxidation induced by Adrenal cells and their subsequent cytotoxicity can be prevented (in part) by antioxidants, and the potential therapeutic use of antioxidants in Wolman disease is discussed.
Yu Fujiwara - One of the best experts on this subject based on the ideXlab platform.
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the first case of thrombocytopenia anasarca fever renal impairment or reticulin fibrosis and organomegaly tafro syndrome with unilateral Adrenal Necrosis a case report
Journal of Medical Case Reports, 2018Co-Authors: Yu Fujiwara, Akito Takamura, Kaoru NagataAbstract:TAFRO syndrome, which was first reported in 2010 in Japan, is a relatively rare disease characterized by thrombocytopenia, anasarca, fever, renal impairment, reticulin fibrosis, and organomegaly. Although this disease is considered similar to multicentric Castleman disease, some of the clinical features, such as thrombocytopenia, are different from typical cases of multicentric Castleman disease. In addition, the etiology of TAFRO syndrome remains unknown and controversial. There have only been a few cases of TAFRO syndrome complicated with Adrenal gland lesions, and all of them have had hemorrhagic involvement. This report describes the case of a 46-year-old Asian man who presented with fever, epigastric pain, and back pain for 1 month. A computed tomographic scan revealed ascites, mild lymphadenopathy, and left Adrenal Necrosis without hemorrhage. A blood test showed thrombocytopenia, anemia, and elevated C-reactive protein, alkaline phosphatase, and creatinine levels. Based on the edema, severe thrombocytopenia, fever, reticulin myelofibrosis shown by bone marrow biopsy, mild lymphadenopathy, and progressive renal insufficiency, we diagnosed this patient as having TAFRO syndrome. He was successfully treated by immediate administration of glucocorticoids and tocilizumab. There have been no previous reports of a case of TAFRO syndrome complicated with Adrenal Necrosis. Because the biopsy of the left Adrenal gland revealed Necrosis without any evidence of hemorrhage, we concluded that the unilateral Adrenal Necrosis in this case was caused by either ischemia from infarction or organomegaly itself under severe hypercytokinemia. This unusual clinical course is useful for further analysis of the etiology of TAFRO syndrome.
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The first case of thrombocytopenia, anasarca, fever, renal impairment or reticulin fibrosis, and organomegaly (TAFRO) syndrome with unilateral Adrenal Necrosis: a case report
Journal of Medical Case Reports, 2018Co-Authors: Yu Fujiwara, Akito Takamura, Kaoru NagataAbstract:Background TAFRO syndrome, which was first reported in 2010 in Japan, is a relatively rare disease characterized by thrombocytopenia, anasarca, fever, renal impairment, reticulin fibrosis, and organomegaly. Although this disease is considered similar to multicentric Castleman disease, some of the clinical features, such as thrombocytopenia, are different from typical cases of multicentric Castleman disease. In addition, the etiology of TAFRO syndrome remains unknown and controversial. There have only been a few cases of TAFRO syndrome complicated with Adrenal gland lesions, and all of them have had hemorrhagic involvement. Case presentation This report describes the case of a 46-year-old Asian man who presented with fever, epigastric pain, and back pain for 1 month. A computed tomographic scan revealed ascites, mild lymphadenopathy, and left Adrenal Necrosis without hemorrhage. A blood test showed thrombocytopenia, anemia, and elevated C-reactive protein, alkaline phosphatase, and creatinine levels. Based on the edema, severe thrombocytopenia, fever, reticulin myelofibrosis shown by bone marrow biopsy, mild lymphadenopathy, and progressive renal insufficiency, we diagnosed this patient as having TAFRO syndrome. He was successfully treated by immediate administration of glucocorticoids and tocilizumab. Conclusions There have been no previous reports of a case of TAFRO syndrome complicated with Adrenal Necrosis. Because the biopsy of the left Adrenal gland revealed Necrosis without any evidence of hemorrhage, we concluded that the unilateral Adrenal Necrosis in this case was caused by either ischemia from infarction or organomegaly itself under severe hypercytokinemia. This unusual clinical course is useful for further analysis of the etiology of TAFRO syndrome.
