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Carlos R Platasalaman - One of the best experts on this subject based on the ideXlab platform.
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interleukin 1β system ligand receptor type i receptor accessory protein and receptor antagonist tnf α tgf β1 and neuropeptide y mrnas in specific brain regions during bacterial lps induced anorexia
Brain Research Bulletin, 1998Co-Authors: Sergey E Ilyin, Dave Gayle, Mark C Flynn, Carlos R PlatasalamanAbstract:Abstract Bacterial lipopolysaccharide (LPS) or endotoxin induces neurological manifestations including anorexia. It is proposed that LPS-induced cytokine production is involved in the generation of neurological manifestations and in neuroinflammatory/immunological responses during Gram-negative infections. For example, LPS-induced effects can be blocked or ameliorated by the interleukin-1 receptor antagonist (IL-1Ra). Here, sensitive and specific RNase protection assays were used to investigate the effects of the intracerebroventricular (i.c.v.) administration of LPS on mRNA levels of interleukin-1β (IL-1β) system components, Tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, and neuropeptide Y (NPY) in the cerebellum, hippocampus, and Hypothalamus. The same brain region sample was analyzed with all of the antisense probes. The data show simultaneous local induction of multiple cytokine components messenger ribonucleic acids (mRNAs) within specific brain regions in anorectic rats responding to i.c.v. administered LPS (500 ng/rat). Interleukin-1β and IL-1Ra had a similar mRNA induction profile (Hypothalamus > cerebellum > hippocampus). Interleukin-1 receptor type I (IL-1RI) mRNA also increased in all three brain regions examined, and the soluble form of IL-1 receptor accessory protein (IL-1R AcP II) mRNA was induced in the Hypothalamus. Tumor necrosis factor-α mRNA levels increased in the Hypothalamus > hippocampus > cerebellum. Levels of membrane bound IL-1R AcP, TGF-β1, and NPY mRNAs did not change significantly in any brain region. The results suggest that: (1) endogenous up-regulation of IL-1β and TNF-α in the Hypothalamus contribute to LPS-induced anorexia; and (2) the ratio IL-1Ra/IL-1β, and IL-1β ↔ TNF-α interactions may have implications for Gram-negative infections associated with high levels of LPS in the brain-cerebrospinal fluid.
Calvo Escribano C - One of the best experts on this subject based on the ideXlab platform.
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Hypogonadotropic hypogonadism in Klinefelter syndrome and hypothalamic-pituitary Tumor
2017Co-Authors: Beisti Ortego A, Calvo Escribano C, De Arriba Muñoz A, Ferrer Lozano,m., Martínez De Zabarte Fernánadez, Jm, Labarta Aizpún J.Abstract:El síndrome de Klinefelter es la causa más frecuente de hipogonadismo hipergonadotropo en el varón. La supresión en la respuesta al estímulo con hormona liberadora de la hormona luteinizante en estos pacientes debe hacer sospechar como posible etiología una Tumoración a nivel hipotalámico. Se presenta el caso de un paciente diagnosticado a los 4 meses con síndrome de Klinefelter mediante cribado neonatal, con cariotipo 47 XXY, en el que se realizan controles clínicos y analíticos seriados y se encuentran, a los 17 años, valores suprimidos de hormona luteinizante y hormona folículo estimulante. Inicia, posteriormente, cefalea y amaurosis de ojo izquierdo, y se encuentra, en una resonancia magnética cerebral, un Tumor germinal mixto a nivel hipotalámico, que precisa tratamiento quirúrgico, quimioterapia y radioterapia, con respuesta favorable. Klinefelter Syndrome is the most frequent cause of hypergonadotropic hypogonadism in men. A flat response at luteinizing hormone releasing hormone stimulation test could be the first sign of hypothalamic Tumor in these patients. We report the case of a patient diagnosed by neonatal screening with Klinefelter Syndrome, 47 XXY, that at 17 years follow-up presents analytical modification of the response to luteinizing hormone releasing hormone stimulation test with suppressed luteinizing hormone and follicle-stimulating hormone values; lately he presents with headache and loss of left eye vision. A magnetic resonance imaging of the brain showed a mixed germ cell Hypothalamus Tumor, requiring surgery, chemotherapy and radiotherapy with optimal response
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Hypogonadotropic hypogonadism in Klinefelter syndrome and hypothalamic-pituitary Tumor
Archivos Argentinos De Pediatria, 2015Co-Authors: Beisti Ortego A, De Arriba Muñoz A, Ferrer Lozano M, Martínez De Zabarte Fernández Jm, Calvo Escribano CAbstract:Abstract Klinefelter Syndrome is the most frequent cause of hypergonadotropic hypogonadism in men. A flat response at luteinizing hormone releasing hormone stimulation test could be the first sign of hypothalamic Tumor in these patients. We report the case of a patient diagnosed by neonatal screening with Klinefelter Syndrome, 47 XXY, that at 17 years follow-up presents analytical modification of the response to luteinizing hormone releasing hormone stimulation test with suppressed luteinizing hormone and follicle-stimulating hormone values; lately he presents with headache and loss of left eye vision. A magnetic resonance imaging of the brain showed a mixed germ cell Hypothalamus Tumor, requiring surgery, chemotherapy and radiotherapy with optimal response.
Beisti Ortego A - One of the best experts on this subject based on the ideXlab platform.
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Hypogonadotropic hypogonadism in Klinefelter syndrome and hypothalamic-pituitary Tumor
2017Co-Authors: Beisti Ortego A, Calvo Escribano C, De Arriba Muñoz A, Ferrer Lozano,m., Martínez De Zabarte Fernánadez, Jm, Labarta Aizpún J.Abstract:El síndrome de Klinefelter es la causa más frecuente de hipogonadismo hipergonadotropo en el varón. La supresión en la respuesta al estímulo con hormona liberadora de la hormona luteinizante en estos pacientes debe hacer sospechar como posible etiología una Tumoración a nivel hipotalámico. Se presenta el caso de un paciente diagnosticado a los 4 meses con síndrome de Klinefelter mediante cribado neonatal, con cariotipo 47 XXY, en el que se realizan controles clínicos y analíticos seriados y se encuentran, a los 17 años, valores suprimidos de hormona luteinizante y hormona folículo estimulante. Inicia, posteriormente, cefalea y amaurosis de ojo izquierdo, y se encuentra, en una resonancia magnética cerebral, un Tumor germinal mixto a nivel hipotalámico, que precisa tratamiento quirúrgico, quimioterapia y radioterapia, con respuesta favorable. Klinefelter Syndrome is the most frequent cause of hypergonadotropic hypogonadism in men. A flat response at luteinizing hormone releasing hormone stimulation test could be the first sign of hypothalamic Tumor in these patients. We report the case of a patient diagnosed by neonatal screening with Klinefelter Syndrome, 47 XXY, that at 17 years follow-up presents analytical modification of the response to luteinizing hormone releasing hormone stimulation test with suppressed luteinizing hormone and follicle-stimulating hormone values; lately he presents with headache and loss of left eye vision. A magnetic resonance imaging of the brain showed a mixed germ cell Hypothalamus Tumor, requiring surgery, chemotherapy and radiotherapy with optimal response
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Hypogonadotropic hypogonadism in Klinefelter syndrome and hypothalamic-pituitary Tumor
Archivos Argentinos De Pediatria, 2015Co-Authors: Beisti Ortego A, De Arriba Muñoz A, Ferrer Lozano M, Martínez De Zabarte Fernández Jm, Calvo Escribano CAbstract:Abstract Klinefelter Syndrome is the most frequent cause of hypergonadotropic hypogonadism in men. A flat response at luteinizing hormone releasing hormone stimulation test could be the first sign of hypothalamic Tumor in these patients. We report the case of a patient diagnosed by neonatal screening with Klinefelter Syndrome, 47 XXY, that at 17 years follow-up presents analytical modification of the response to luteinizing hormone releasing hormone stimulation test with suppressed luteinizing hormone and follicle-stimulating hormone values; lately he presents with headache and loss of left eye vision. A magnetic resonance imaging of the brain showed a mixed germ cell Hypothalamus Tumor, requiring surgery, chemotherapy and radiotherapy with optimal response.
Labarta Aizpún J. - One of the best experts on this subject based on the ideXlab platform.
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Hypogonadotropic hypogonadism in Klinefelter syndrome and hypothalamic-pituitary Tumor
2017Co-Authors: Beisti Ortego A, Calvo Escribano C, De Arriba Muñoz A, Ferrer Lozano,m., Martínez De Zabarte Fernánadez, Jm, Labarta Aizpún J.Abstract:El síndrome de Klinefelter es la causa más frecuente de hipogonadismo hipergonadotropo en el varón. La supresión en la respuesta al estímulo con hormona liberadora de la hormona luteinizante en estos pacientes debe hacer sospechar como posible etiología una Tumoración a nivel hipotalámico. Se presenta el caso de un paciente diagnosticado a los 4 meses con síndrome de Klinefelter mediante cribado neonatal, con cariotipo 47 XXY, en el que se realizan controles clínicos y analíticos seriados y se encuentran, a los 17 años, valores suprimidos de hormona luteinizante y hormona folículo estimulante. Inicia, posteriormente, cefalea y amaurosis de ojo izquierdo, y se encuentra, en una resonancia magnética cerebral, un Tumor germinal mixto a nivel hipotalámico, que precisa tratamiento quirúrgico, quimioterapia y radioterapia, con respuesta favorable. Klinefelter Syndrome is the most frequent cause of hypergonadotropic hypogonadism in men. A flat response at luteinizing hormone releasing hormone stimulation test could be the first sign of hypothalamic Tumor in these patients. We report the case of a patient diagnosed by neonatal screening with Klinefelter Syndrome, 47 XXY, that at 17 years follow-up presents analytical modification of the response to luteinizing hormone releasing hormone stimulation test with suppressed luteinizing hormone and follicle-stimulating hormone values; lately he presents with headache and loss of left eye vision. A magnetic resonance imaging of the brain showed a mixed germ cell Hypothalamus Tumor, requiring surgery, chemotherapy and radiotherapy with optimal response
Sergey E Ilyin - One of the best experts on this subject based on the ideXlab platform.
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interleukin 1β system ligand receptor type i receptor accessory protein and receptor antagonist tnf α tgf β1 and neuropeptide y mrnas in specific brain regions during bacterial lps induced anorexia
Brain Research Bulletin, 1998Co-Authors: Sergey E Ilyin, Dave Gayle, Mark C Flynn, Carlos R PlatasalamanAbstract:Abstract Bacterial lipopolysaccharide (LPS) or endotoxin induces neurological manifestations including anorexia. It is proposed that LPS-induced cytokine production is involved in the generation of neurological manifestations and in neuroinflammatory/immunological responses during Gram-negative infections. For example, LPS-induced effects can be blocked or ameliorated by the interleukin-1 receptor antagonist (IL-1Ra). Here, sensitive and specific RNase protection assays were used to investigate the effects of the intracerebroventricular (i.c.v.) administration of LPS on mRNA levels of interleukin-1β (IL-1β) system components, Tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β1, and neuropeptide Y (NPY) in the cerebellum, hippocampus, and Hypothalamus. The same brain region sample was analyzed with all of the antisense probes. The data show simultaneous local induction of multiple cytokine components messenger ribonucleic acids (mRNAs) within specific brain regions in anorectic rats responding to i.c.v. administered LPS (500 ng/rat). Interleukin-1β and IL-1Ra had a similar mRNA induction profile (Hypothalamus > cerebellum > hippocampus). Interleukin-1 receptor type I (IL-1RI) mRNA also increased in all three brain regions examined, and the soluble form of IL-1 receptor accessory protein (IL-1R AcP II) mRNA was induced in the Hypothalamus. Tumor necrosis factor-α mRNA levels increased in the Hypothalamus > hippocampus > cerebellum. Levels of membrane bound IL-1R AcP, TGF-β1, and NPY mRNAs did not change significantly in any brain region. The results suggest that: (1) endogenous up-regulation of IL-1β and TNF-α in the Hypothalamus contribute to LPS-induced anorexia; and (2) the ratio IL-1Ra/IL-1β, and IL-1β ↔ TNF-α interactions may have implications for Gram-negative infections associated with high levels of LPS in the brain-cerebrospinal fluid.