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  • Digitale Medien  (19)
  • Immunohistochemistry  (6)
  • Edema  (5)
  • Spinal cord injury  (5)
  • Agropyron  (3)
  • Heat stress  (3)
  • vitamin A  (3)
Materialart
  • Digitale Medien  (19)
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  • 1
    ISSN: 1436-6215
    Schlagwort(e): RBP secretion ; vitamin A ; carotenoids ; goat ; RBP-Sekretion ; Vitamin A ; Carotinoide ; Ziege
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Land- und Forstwirtschaft, Gartenbau, Fischereiwirtschaft, Hauswirtschaft , Medizin
    Beschreibung / Inhaltsverzeichnis: Zusammenfassung Die Sekretion von retinolbindendem Protein (RBP) ins Blut von Ziegen wurde nach unterschiedlicher Verabreichung von Vitamin A (Retinylacetat), Β-Carotin und einer Mischung von pflanzlichen Carotinoiden untersucht. Die Zufuhr dieser Verbindungen — entweder in einer einzelnen hohen Dosis oder in der gleichen Menge gleichmäßig auf 4 Tagesdosen verteilt — führte zu einem deutlichen Anstieg der RBP-Sekretion. Diese Sekretion erfolgte in zwei Phasen, von denen eine früh und eine später einsetzte.
    Notizen: Summary Studies were conducted on the secretion of retinol-binding protein (RBP) in blood of goats given different treatments of preformed vitamin A, Β-carotene and plant carotenoids. Administration of these sources either in a single massive dose or massive dose split into four equal doses, markedly increased the secretion of RBP in blood. The secretion of RBP in blood occurred at least in two phases, one at early periods and the other at later periods.
    Materialart: Digitale Medien
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Cellular and molecular life sciences 46 (1990), S. 208-211 
    ISSN: 1420-9071
    Schlagwort(e): Brain development ; DNA ; RNA ; protein ; vitamin A ; rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Summary The biochemical development of the fetal brain in relation to maternal vitamin A restriction was studied in rats. The vitamin A status of pregnant rats was varied by supplying low, medium and adequate amounts (6, 40, and 100 μg retinol/day/kg body weight, respectively) of vitamin A during pregnancy and suckling. The maternal vitamin A restriction caused an altered brain development in terms of tissue weight, DNA, RNA and protein levels, and biosynthesis of DNA and protein from [3H]-thymidine and [3H]-leucine, respectively. A dose-dependent effect of maternal vitamin A restriction on the metabolism of DNA, RNA and protein was noticed in the developing fetal brain of rats.
    Materialart: Digitale Medien
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  • 3
    ISSN: 1438-2199
    Schlagwort(e): Keywords: Amino acids ; Growth hormone ; Spinal cord injury ; Edema formation ; Spinal cord evoked potentials ; Spinal cord edema ; Cell injury
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary. The influence of exogenous rat growth hormone on spinal cord injury induced alterations in spinal cord evoked potentials (SCEP) and edema formation was examined in a rat model. Repeated topical application of rat growth hormone (20 μl of 1 μg/ml solution) applied 30 min before injuryand at 0 min (at the time of injury), 10 min, 30 min, 60 min, 120 min, 180 min, and 240 min, resulted in a marked preservation of SCEP amplitude after injury. In addition, the treated traumatised cord showed significantly less edema and cell changes. These observations suggest that growth hormone has the capacity to improve spinal cord conduction and attenuate edema formation and cell injury in the cord indicating a potential therapeutic implication of this peptide in spinal cord injuries.
    Materialart: Digitale Medien
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  • 4
    ISSN: 1438-2199
    Schlagwort(e): Keywords: Amino acids ; Spinal cord injury ; Heme oxygenase ; Heat shock protein ; Carbon monoxide ; Growth factors ; BDNF ; IGF-1 ; Immunohistochemistry ; Cell injury ; Spinal cord edema
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary. The influence of brain derived neurotrophic factor (BDNF) or insulin like growth factor-1 (IGF-1) on spinal cord trauma induced carbon monoxide (CO) production and cellular stress response was examined using immunostaining of the constitutive isoform of the hemeoxygenase (HO-2) enzyme and the heat shock protein (HSP 72 kD) expression in a rat model. Subjection of rats to a 5 h spinal trauma inflicted by an incision into the right dorsal horn at T10–11 segment markedly upregulated the HO-2 and HSP expression in the adjacent spinal cord segments (T9 and T12). Pretreatment with BDNF or IGF-1 significantly attenuated the trauma induced HSP expression. The upregulation of HO-2 was also considerably reduced. These results show that BDNF and IGF-1 attenuate cellular stress response and production of CO following spinal cord injury which seems to be the key factors in neurotrophins induced neuroprotection.
    Materialart: Digitale Medien
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  • 5
    ISSN: 1438-2199
    Schlagwort(e): Heat stress ; Nitric oxide ; Cell injury ; Antioxidant ; H-290/51Blood-brain barrier ; Brain edema
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that nitric oxide (NO) is involved in the pathophysiology of brain injury caused by heat stress (HS) was examined using neuronal nitric oxide synthase (NOS) immunohistochemistry in a rat model. In addition, to find out a role of oxidative stress in NOS upregulation and cell injury, the effect of a new antioxidant compound H-290/51 (Astra Hässle, Mälndal, Sweden) was examined in this model. Subjection of conscious young rats to 4 h HS in a biological oxygen demand (BOD) incubator at 38°C resulted in a marked upregulation of NOS in many brain regions compared to control rats kept at room temperature (21 ± 1°C. This NOS immunoreactivity was found mainly in distorted neurons located in the edematous regions not normally showing NOS activity. Breakdown of the blood-brain barrier (BBB) permeability, increase in brain water content and marked neuronal, glial and myelin reaction were common findings in several brain regions exhibiting upregulation of NOS activity. Pretreatment with H-290/51 significantly attenuated the upregulation of NOS in rats subjected to HS. In these animals breakdown of the BBB permeability, edema and cell changes were considerably reduced. Our results suggest that hyperthermic brain injury is associated with a marked upregulation of NOS activity in the CNS and this upregulation of NOS and concomitant cell injury can be reduced by prior treatment with an antioxidant compound H 290/51. These observations indicate that oxidative stress seems to be an important endogenous signals for NOS upregulation and cell reaction in hyperthermic brain injury.
    Materialart: Digitale Medien
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  • 6
    ISSN: 1438-2199
    Schlagwort(e): Nitric oxide ; Spinal cord evoked potentials ; Edema ; Cell changes ; p-CPA ; Diazepam ; Immunohistochemistry
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10–11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1h. However, a significant increase in SCEP latency was seen at the end of 5h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.
    Materialart: Digitale Medien
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  • 7
    ISSN: 1438-2199
    Schlagwort(e): Brain derived neurotrophic factor ; Insulin like growth factor-1 ; Nitric oxide ; Spinal cord injury ; Edema ; Cell injury ; Blood-spinal cord barrier ; Immunohistochemistry
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that brain derived neurotrophic factor (BDNF) and insulin like growth factor-1 (IGF) induced neuroprotectivn is influenced by mechanisms involving nitric oxide was examined in a rat model of focal spinal cord injury. BDNF or IGF-I (0.1 μg/10 [1 in phosphate buffer saline) was applied topically 30 min before injury on the exposed spinal cord followed by repeated doses of growth factors immediately before and 30 min after injury. Thereafter application of BDNF or IGF was carried out at every 1 h interval until sacrifice. Five hours after injury, the tissue pieces from the T9 segment were processed for nNOS immunostaining, edema and cell injury. Untreated injured rats showed a profound upregulation of nNOS which was most pronounced in the nerve cells of the ipsilateral side. A marked increase in the blood-spinal cord barrier (BSCB) permeability to125I-albumin, water content and cell injury in these perifocal segments was also found. Pretreatment with BDNF and IGF significantly reduced the upregulation of nNOS in the spinal cord. This effect of the growth factors was most pronounced in the contralateral side. Rats treated with these neurotrophic factors showed much less signs of BSCB damage, edema and cell injury. These results suggest that BDNF and IGF pretreatment is neuroprotective in spinal cord injury and that these neurotrophic factors have the capacity to down regulate nNOS expression following trauma to the spinal cord. Our data provide new experimental evidences which suggest that BDNF and IGF may exert their potential neuroprotective effects probably via regulation of NOS activity.
    Materialart: Digitale Medien
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  • 8
    Digitale Medien
    Digitale Medien
    Springer
    European journal of nutrition 26 (1987), S. 116-124 
    ISSN: 1436-6215
    Schlagwort(e): lung ; development ; vitamin A ; DNA ; RNA ; protein ; rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Land- und Forstwirtschaft, Gartenbau, Fischereiwirtschaft, Hauswirtschaft , Medizin
    Beschreibung / Inhaltsverzeichnis: Zusammenfassung Der Einfluß einer Beschränkung der Vitamin-A-Zufuhr für das Muttertier auf die biochemische Entwicklung der Lunge des Jungtieres wurde bei Ratten untersucht. Der Vitamin-A-Status der Muttertiere wurde durch niedrige, mittlere und adäquate Gaben von Vitamin A während Trächtigkeit und Säugezeit variiert (6, 40 und 100 μg Retinol/Tag/kg Körpergewicht). Die Ergebnisse zeigen, daß die Beschränkung der Vitamin-A-Zufuhr für das Muttertier das Wachstum und die Entwicklung der Lunge in bezug auf Gewicht, DNA- und Proteingehalt und -biosynthese aus markierten Vorstufen, RNA-Gehalt, Zellgröße und Zellzahl beeinflussen.
    Notizen: Summary The effect of maternal vitamin A restriction on the biochemical development of the lung in rats has been studied. The vitamin A status of dams has been varied by supplying low, medium and adequate amounts of vitamin A (6, 40 and 100 μg retinol/day/kg body weight, respectively) during pregnancy and suckling. The results demonstrate that the restricted supply of vitamin A to the mother affected the growth and development of the lung in parameters of tissue weight, DNA and protein levels and their biosynthesis from respective labelled precursors, RNA contents, cell number and cell size.
    Materialart: Digitale Medien
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  • 9
    Digitale Medien
    Digitale Medien
    Springer
    Acta neuropathologica 79 (1990), S. 595-603 
    ISSN: 1432-0533
    Schlagwort(e): Trauma ; Spinal cord injury ; Microvascular permeability ; Serotonin ; p-Chlorophenylalanine (p-CPA)
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that serotonin can take part in the initiation of the increased microvascular permeability occurring in a spinal cord trauma was investigated in a rat model with 131I-sodium and lanthanum as tracers. We influenced the serotonin content in the tissue pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA), before the production of the injury and compared the results with injured, untreated controls. A small incision was made in the dorsal horn of the lower thoracic cord. It caused a progressive extravasation of 131I-sodium in the damaged segment, measured after 1,2 and 5 h. Rostral and caudal segments also showed a significant but lower accumulation of 131I-sodium. Lanthanum added to the fixative was used as an ionic tracer detectable by electron microscopy. The endothelial cells of microvessels removed from the perifocal region after 5 h showed a marked increase in the number of lanthanum-filled vesicles. Many endothelial cells had a diffuse penetration of the tracer into the cytoplasm and the basement membrane. However, the tight junctions usually remained closed to lanthanum. Pretreatment with p-CPA markedly reduced the extravasation of 131I-sodium measured at 5 h in the traumatized cord. At the cellular level, the endothelial vesicles filled with lanthanum approached the condition of uninjured animals. The diffuse infiltration of lanthanum into endothelial cells and its spread into the basement membrane of the vascular wall were usually absent. Our results indicate that serotonin plays a role in the initiation of the increased microvascular permeability which occurs in spinal cord injuries.
    Materialart: Digitale Medien
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  • 10
    Digitale Medien
    Digitale Medien
    Springer
    Acta neuropathologica 79 (1990), S. 604-610 
    ISSN: 1432-0533
    Schlagwort(e): Trauma ; Spinal cord injury ; Edema ; Serotonin ; p-CPA
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that serotonin can modify the early pathological sequences occurring in spinal cord trauma was investigated in a rat model. To that end we took advantage of the possibility of influencing serotonin pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before the production of the injury and compared the results with injured, untreated controls. A unilateral incision was made into the dorsal horn of the lower thoracic cord (about 2.5 mm deep, 4.5 mm long) and the trauma. The injured region from untreated animals showed macroscopically at that time a pronounced swelling and the water content had increased by 3.5% as compared to intact controls. The segments rostral and caudal to the lesion also exhibited a profound increase in water content. Light microscopy revealed a significant expansion of the spinal cord as compared to controls. The swelling was most pronounced in the gray matter on the injured side. Electron microscopy showed distorted neurons, swollen astrocytes and extracellular edema in the gray matter in and around the primary lesion. There was also a sponginess in the surrounding white matter with disruption of myelin, collapsed axons and widened periaxonal spaces. Pretreatment of the rats with p-CPA significantly reduced the swelling of the injured spinal cord and there was no visible expansion. The ipsilateral edema in the central gray matter was considerable less pronounced as compared to that in untreated animals. The increase in water content was less than 1% in these animals. The neuronal and glial cell changes were also markedly reduced in the drugtreated rats. The disruption of myelin and the vacuolation of the gray matter were much less severe. Our results show that p-CPA can markedly modify the edema and the cellular changes occurring in the traumatic spinal injury and indicate that serotonin is somehow involved in the production of the early, and thus important, pathological events.
    Materialart: Digitale Medien
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