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J Szaflarski

Publications and source records attributed to J Szaflarski.

At least 19 recordsLinked to original sources
PubMed2000

Monocyte chemoattractant protein-1 is a mediator of acute excitotoxic injury in neonatal rat brain.

Monocyte chemoattractant protein-1 is a chemokine with potent monocyte activating and chemotactic effects. Monocyte chemoattractant protein-1 gene and protein expression is rapidly up-regulated in response to a variety of acute and chronic central nervous system disorders. The activation and recruitment of microglia and monocytes into areas of inflammation may play a critical role in the pathogenesis of acute brain injury. Monocyte chemoattractant protein-1 could be a pathophysiologically important mediator of the microglial and monocyte responses in the brain. Using a well-characterized model of acute excitotoxic brain injury in neonatal rats, experiments were designed to evaluate whether monocyte chemoattractant protein-1 plays a role in the progression of tissue damage. Direct co-administration of recombinant monocyte chemoattractant protein-1 with the excitotoxin N-methyl-D-aspartate exacerbated injury, both in the striatum and in the hippocampus, by 55% and 167%, respectively. Complementary experiments to determine the effect of functional inhibition of monocyte chemoattractant protein-1, using an anti-monocyte chemoattractant protein-1-neutralizing antibody, revealed that co-administration of the antibody with N-methyl-D-aspartate attenuated tissue injury in the striatum and hippocampus by 57% and 39%, respectively.Together, these data suggest that monocyte chemoattractant protein-1 is a mediator of acute excitotoxic brain injury in neonatal rats and that inflammatory mechanisms contribute significantly to the pathogenesis of acute neonatal brain injury. Whether chemokines are pathophysiologically relevant mediators of neuronal injury in human neonates remains to be determined.

Acute Disease↗
PubMed1998

Excitotoxic injury induces monocyte chemoattractant protein-1 expression in neonatal rat brain.

Intra-hippocampal injection of NMDA (12.5 nmol) in postnatal day 7 (P7) rats results in neuronal necrosis and hippocampal atrophy; injury extends into the adjacent striatum, thalamus and cortex. NMDA-induced injury is marked by an acute microglial/monocyte response; the molecular signals that control this response and the role of activated microglia/monocytes in the progression of excitotoxic injury are unknown. Monocyte chemoattractant protein-1 (MCP-1) is a well-characterized chemokine that regulates monocyte chemotaxis and activation, and contributes to the pathogenesis of monocyte-dependent tissue injury in several disease models. We hypothesized that MCP-1 could be a regulator of the microglial/monocyte response to excitotoxic injury in neonatal rat brain. To determine if intra-hippocampal NMDA injections induced MCP-1 mRNA expression, in situ hybridization assays were performed in brain samples obtained from 7-day-old rats, evaluated 0-24 h after intra-hippocampal NMDA injection. MCP-1 mRNA expression was first detected at 2 h after lesioning, in the choroid fissure, adjacent to the lesioned hippocampus; levels of expression increased markedly in the lesioned hippocampus and adjacent structures within the first 16 h after NMDA injection, and then rapidly declined. In control animals that received intra-hippocampal saline injections, only minimal MCP-1 mRNA was detected, along the injection track. These results demonstrate that excitotoxic injury transiently induces MCP-1 gene expression in neonatal rat brain. The functional role of MCP-1 in the injured brain remains to be determined.

Animals↗
PubMed1997

Hypoxic-ischemic injury induces monocyte chemoattractant protein-1 expression in neonatal rat brain.

Monocyte chemoattractant protein-1 (MCP-1) regulates monocyte accumulation in several macrophage-dependent experimental disease models. In the neonatal brain, activated microglia accumulate rapidly after hypoxic-ischemic injury. These cells produce potentially neurotoxic factors that may contribute to the progression of injury. To determine whether MCP-1 could be one of the molecular signals that influences the microglial response to hypoxic-ischemic injury in the neonatal brain, we examined the impact of acute hypoxic-ischemic injury on MCP-1 mRNA and protein expression. Seven-day-old rats underwent right carotid artery ligation, followed by 3 hours of 8% oxygen exposure, to elicit ipsilateral forebrain hypoxic-ischemic injury. To detect MCP-1 mRNA in situ hybridization assays were performed using 35S-labeled antisense riboprobes generated from rat MCP-1 cDNA. Animals were evaluated 0, 1, 2, 4, 8, 16, 24, 48, and 120 hours after hypoxic exposure (N > or = 3/group). Immunocytochemistry (with a polyclonal rabbit antirat MCP-1 antibody) was used to determine the anatomic and temporal distribution of MCP-1, in samples obtained 10 minutes to 5 days after hypoxic exposure (N > or = 3/group). Monocyte chemoattractant protein-1 mRNA was first detected in periventricular regions of the lesioned hemisphere 1 hour after hypoxia-ischemia; periependymal and intraparenchymal MCP-1 mRNA expression were detected at 4 hours; hybridization signal peaked at 8 to 24 hours; and no MCP-1 mRNA was detected at 48 and 120 hours. In lesioned forebrain, MCP-1 protein expression were consistently detected at 2.5 to 48 hours after hypoxia-ischemia. Many immunoreactive cells appeared to be neurons. These results suggest that in the developing brain, MCP-1 could represent a functionally important molecular signal for the microglial response to hypoxic-ischemic injury.

Animals↗
PubMed1995

Cerebral hypoxia-ischemia stimulates cytokine gene expression in perinatal rats.

BACKGROUND AND PURPOSE: We tested the hypothesis that cerebral hypoxia-ischemia selectively stimulates interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) gene expression in brain regions susceptible to irreversible injury in perinatal rats. METHODS: To elicit focal hypoxic-ischemic brain injury, 7-day-old perinatal (P7) rats were subjected to right carotid artery ligation followed by 3 hours of 8% O2 exposure and were killed 0 to 48 hours after hypoxia. Regional tissue IL-1 beta and TNF-alpha mRNA content were measured by reverse transcription followed by polymerase chain reaction amplification (RT-PCR) in samples prepared from cortex and hippocampus of the lesioned and contralateral hemispheres. cDNAs were amplified with primers specific for IL-1 beta, TNF-alpha, and the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which served as an internal control. The RT-PCR products were subjected to Southern blot analysis and hybridized with 32P-labeled gene-specific probes. Radioactivity was measured in excised bands, and results were normalized on the basis of levels of GAPDH expression. RESULTS: In unlesioned P7 brain, IL-1 beta mRNA was barely detectable. In lesioned forebrain, there was a marked, transient stimulation of IL-1 beta mRNA expression, peaking at 4 hours after hypoxia. Hybridization signal was increased 16- to 30-fold over values from contralateral hemisphere samples in three independent assays (P < .05 comparing values in left and right cortex and in left and right hippocampus with the Kruskal-Wallis ranking test); by 24 hours after hypoxia, levels returned to normal. Similar transient increases in TNF-alpha mRNA expression were detected. In a closely related model of perinatal brain injury elicited by focal intracerebral N-methyl-D-aspartate injection, there was a corresponding acute stimulation of IL-1 beta and TNF-alpha mRNA expression at 4 hours after injection. CONCLUSIONS: These results suggest that IL-1 beta and TNF-alpha may play important roles in the response of the developing brain to acute hypoxic-ischemic injury.

Animals↗
PubMed1993

[An attempt to estimate epidemiologic prevalence of HBs associated antigen among hospitalized children].

We have observed the problem of the more frequent occurrence of the hepatitis-associated antigen (HBsAg) among multiple hospitalized children and we have analysed the medical documentation of children who were treated in the Department of Gastroenterology and Pediatrics of the Medical Academy of Bydgoszcz in 1989-1992 years. In this period of time we have recorded 39 children with HBsAg. In 80% (31 patients) there are children, who were hospitalized two or more times. We have proved, that in the group of children with HBsAg, children with chronic illness or frequently hospitalized were the risk group.

Child↗
PubMed1977

Biological properties and clinical application of propolis. I. Some physico-chemical properties of propolis.

The presence of 19 elements has been shown in the ethanol extracts of propolis (EEP). Three fractions have been obtained by filtration through a structural gel that did not show an initial antibacterial activity when investigated separately. Fractions 2 and 3 joined together have regained this activity. EEP solutions maintain their anitbacterial activity in acidic or neutral pH. Insensitivity of EEP solutions on temperautre of 75 degrees C for 30 min has been found.

Bees↗
PubMed1976

A trial of using antibodies as carriers of alkylating agents. II. Evaluation of ability to form 32P-cyclophosphamide + immune antibody complexes with homologous antigen.

32P-cyclophosphamide was found to combine with gamma-globulin fractions of immune sera. Immune sera incubated with 32P-cyclophosphamide retained ability to react specifically with homologous antigen in vitro in the system: MN antigens of human erythrocytes + rabbit anti-MN antibody, and probably reacted selectively with target antigens in vivo in the system: antigens of guinea pig kidney tissue + rabbit antibodies against these antigens. Hemagglutination, passive hemagglutination and precipitation in agar gel tests were used in the experiments. Ability to combine of the immune antibody + 32P-cyclophosphamide complex with homologous antigens was evaluated by measurements of radioactivity of studied materials (erythrocyte agglutinates and organ homogenates). The results indicate feasibility of using immune antibodies as carriers of cytostatic agents.

Alkylating Agents↗
PubMed1975

A trial of utilizing antibodies as carriers of alkylating agents. I. Influence of cyclophosphamide and chlormethine on antigenic properties of serum proteins.

Electrophorograms of human and rabbit sera before and after incubation with various concentrations of cyclophosphamide and chlormethine (Nitrogranulogen) were compared. Sera of rabbits injected with chlormethine and cyclophosphamide in therapeutic doses for humans were examined for antibodies reacting with homologous and antologous gamma-globulins. Immunoelectrophorograms of sera incubated with both alkylating agents differed from those of preincubation sera with regard to number and intensity of precipitin lines. The changes in electrophorograms were related to the type and concentration of alkylating agent. No antibodies to homologous or autologous serum antigens of rabbits treated with chlormethine or cyclophosphamide were found.

Animals↗
PubMed1973

Toxoplasmosis.

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History, 20th Century↗