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1

Acute ischaemic stroke increases the erythrocyte sedimentation rate, which correlates with early brain damage

100%

Zaremba J., Skrobanski P., Losy J.

Folia Morphologica

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2004

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tom 63

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nr 4

The acute phase response follows tissue injury and contributes to its exacerbation with pro-inflammatory and pro-thrombotic mechanisms. Acute phase proteins promote erythrocyte aggregation and falling, with the result that the erythrocyte sedimentation rate (ESR) is a measure of the acute phase response. As the acute phase response accompanies ischaemic brain damage, we studied ESR values in patients within the first 24 hours of ischaemic stroke and evaluated whether these values may be related to the volume of anatomically relevant single hemispheric brain computed tomography (CT) areas observed at the same period, indicating early stroke-related cerebral changes. We observed an increase in ESR in stroke patients and a positive correlation between the ESR values and the volume of early brain CT hypodense areas. The results suggest that elevation in ESR values is observed soon after a stroke and may reflect the relationship between the degree of acute phase response in the early phase of ischaemic stroke and the extent of local brain damage.

2

High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

72%

Ilic S., Drmic D., Zarkovic K., Kolenc D., Coric M., Brcic L., Klicek R., Radic B., Sever M., Djuzel V., Ivica M., Boban Blagaic A., Zoricic Z., Anic T., Zoricic I., Djidic S., Romic Z., Seiwerth S., Sikiric P.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

We focused on stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419, an anti-ulcer peptide efficient in inflammatory bowel disease trials (PL 14736), no toxicity reported) because of its hepatoprotective effects. We investigate a particular aspect of the sudden onset of encephalopathy with extreme paracetamol overdose (5 g/kg intraperitoneally) so far not reported: rapidly induced progressive hepatic encephalopathy with generalized convulsions in rats. BPC 157 therapy (10 µg, 10 ng, 10 pg/kg, intraperitoneally or intragastrically) was effective (µg-ng range) against paracetamol toxicity, given in early (BPC 157 immediately after paracetamol, prophylactically) or advanced stage (BPC 157 at 3 hours after paracetamol, therapeutically). At 25 min post-paracetamol increased ALT, AST and ammonium serum values precede liver lesion while in several brain areas, significant damage became apparent, accompanied by generalized convulsions. Through the next 5 hour seizure period and thereafter, the brain damage, liver damage enzyme values and hyperammonemia increased, particularly throughout the 3-24 h post-paracetamol period. BPC 157 demonstrated clinical (no convulsions (prophylactic application) or convulsions rapidly disappeared (therapeutic effect within 25 min)), microscopical (markedly less liver and brain lesions) and biochemical (enzyme and ammonium serum levels decreased) counteraction. Both, the prophylactic and therapeutic benefits (intraperitoneally and intragastrically) clearly imply BPC 157 (µg-ng range) as a highly effective paracetamol antidote even against highly advanced damaging processes induced by an extreme paracetamol over-dose.

3

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

72%

Dragun P., Makarewicz D., Wojcik L., Ziemka-Nalecz M., Slomka M., Zalewska T.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 3

441-455

Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and carry out key functions during brain development. Apart from a physiological role, excessive activation of MMPs in brain tissue has been postulated to represent a pathway for cell death arising from ischemia. To evaluate the possible involvement of MMPs in the perinatal brain asphyxia, we exposed 7-day-old rats to hypoxia-ischemia (HI). Unilateral HI was administered by ligation of the common carotid artery followed by hypoxia (7.4% O2/92.6% N2) for 65 minutes. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in > 90% of animals. HI resulted in a significant elevation of MMP-2 and MMP-9 activity in the ipsilateral forebrain. The maximum activation was found at 48 hours and 7-14 days after the insult. These results suggest that early and late induction of MMPs may play a role in neuronal death as well as in repair processes. The treatment of animals subjected to HI with 1-methylnicotinamide (MNA), the anti-inflammatory agent, led to the inhibition of MMP-9 in an acute phase of ischemic damage and to the activation of MMP-2 in the later stages after injury. The timing of MMPs modulation by MNA may indicate its possible therapeutic implications.

4

Positron emission tomography findings in obstructive sleep apnea patients with residual sleepiness treated with continuous positive airway pressure

72%

Antczak J., Popp R., Hajak G., Zulley J., Marienhagen J., Geisler P.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 5

5

Signals mediating Klotho-induced neuroprotection in hippocampal neuronal cells

72%

Cheng M.-F., Chen L.-J., Niu H.-S., Yang T.-T., Lin K.-C., Cheng J.-T.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 1

The erythropoietin (Epo) receptor (EpoR) is expressed in the brain and was shown to have neuroprotective effects against brain damage in animal models. A recent study indicated that EpoR and its activity are the downstream effectors of Klotho for cytoprotection in the kidney. Thus, we propose that Klotho can stimulate the expression of EpoR in neuronal cells to enhance Epo-mediated protection. H19-7 hippocampal neuronal cells were treated with recombinant Klotho. In H19-7 cells, Klotho increased the expression of both the EpoR protein and mRNA. Klotho also enhanced the transcription activity of the EpoR promoter in H19-7 cells. Moreover, Klotho augmented the Epo-triggered phosphorylation of Jak2 and Stat5 and protected H19-7 cells from hydrogen peroxide cytotoxicity. The silencing of EpoR abolished the protective effect of Klotho against peroxide-induced cytotoxicity. Finally, the silencing of GATA1 diminished the Klotho-induced increase in EpoR protein and mRNA expression as well as its promoter activity. In conclusion, Klotho increased EpoR expression in neuronal cells through GATA1, thereby enabling EpoR to function as a cytoprotective protein against oxidative injury.

6

Disturbances in time limited storage of sensory information after right temporal lobectomy

72%

Szatkowska I., Szymanska O., Bednarek D., Skowronska R., Grabowska A.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

|

nr 1

7

Immunosuppressants as novel anti-inflammatory drugs affecting MAPK signalling pathways

72%

Kaminska B.

Cellular and Molecular Biology Letters

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2005

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tom 10

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nr Suppl.2

8

How does trimethyltin affect the brain: facts and hypotheses

72%

Koczyk D.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

|

nr 2

9

Cerebellar abnormality in autism: a nonspecific effect of early brain damage?

72%

Ciesielski K. T., Knight J. E.

Acta Neurobiologiae Experimentalis

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1994

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tom 54

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nr 2

10

Memory impairment in patients with stereotaxic lesions to the hippocampus and amygdala

58%

Grabowska A., Luczywek E., Fersten E., Herman A., Szatkowska I.

Acta Neurobiologiae Experimentalis

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1994

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tom 54

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nr 4

11

Zmiany statusu antyoksydacyjnego w korze mozgowej czlowieka po zatruciu heroina

37%

Gutowicz M., Cholojczyk M., Siwinska-Ziolkowska A., Pokorska-Lis M., Szymczakowski S., Sadurska B., Baranczyk-Kuzma A.

Bromatologia i Chemia Toksykologiczna

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2004

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tom 37

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nr 3

277-282

W pracy przedstawiono aktywność seleno-niezależnej peroksydazy glutationowej i katalazy, poziom zredukowanego glutationu, dialdehydu malonowego i grup karbonylowych W rożnych częściach kory mózgowej człowieka. Badania prowadzono na tkankach otrzymywanych z autopsji osób zmarłych na skutek zatrucia heroiną

Ograniczanie wyników

Acute ischaemic stroke increases the erythrocyte sedimentation rate, which correlates with early brain damage

High hepatotoxic dose of paracetamol produces generalized convulsions and brain damage in rats. A counteraction with the stable gastric pentadecapeptide BPC 157 (PL 14736)

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

Positron emission tomography findings in obstructive sleep apnea patients with residual sleepiness treated with continuous positive airway pressure

Signals mediating Klotho-induced neuroprotection in hippocampal neuronal cells

Disturbances in time limited storage of sensory information after right temporal lobectomy

Immunosuppressants as novel anti-inflammatory drugs affecting MAPK signalling pathways

How does trimethyltin affect the brain: facts and hypotheses

Cerebellar abnormality in autism: a nonspecific effect of early brain damage?

Memory impairment in patients with stereotaxic lesions to the hippocampus and amygdala

Zmiany statusu antyoksydacyjnego w korze mozgowej czlowieka po zatruciu heroina