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J Zaremba

Publications and source records attributed to J Zaremba.

At least 19 recordsLinked to original sources
PubMed2006

The level of chemokine CXCL5 in the cerebrospinal fluid is increased during the first 24 hours of ischaemic stroke and correlates with the size of early brain damage.

Inflammation is an important feature of the pathophysiological response to ischaemic stroke. The ischaemic brain-invading leukocytes, neutrophils in particular, contribute to the exacerbation of tissue injury in stroke. Chemokines are a growing family of proteins performing chemotactic activity on selective leukocyte subpopulations. Chemokines are broadly divided into two major subfamilies on the basis of the arrangement of the two N-terminal cysteine residues, CXC and CC, depending on whether the first two cysteine residues have an amino acid between them (CXC) or are adjacent (CC). CXC chemokines possessing, close to the N terminus, the amino acid sequence glutamic acid-leucine-arginine (ELR motif) specifically act on neutrophils. CXCL5 is one of the ELR-expressing CXC chemokines and is a potent neutrophil attractant and activator. The objective of the study was to detect CXCL5 levels in the cerebrospinal fluid (CSF) and sera of stroke patients and to investigate the relation between these levels and the volume of brain computed tomography (CT) hypodense areas representing early ischaemic lesions. A total of 23 ischaemic stroke patients were studied. CSF and blood sampling and brain CT were performed within the first 24 hours of stroke. The control group consisted of 15 patients with tension headache. CXCL5 levels were determined by the ELISA method. CSF CXCL5 levels in stroke patients were significantly higher in comparison with the control group (38.2 +/- 18.4 pg/ml vs. 18.7 +/- 8.2 pg/ml; p < 0.001). No significant differences in serum CXCL5 levels were found between the stroke patients and the control group. CSF CXCL5 levels correlated positively with the volume of early brain CT hypodense areas (p < 0.0001). The results suggest that CXCL5 may play a role in the inflammatory reaction during the early phase of ischaemic stroke.

Acute Disease↗
PubMed2003

Interleukin-18 in acute ischaemic stroke patients.

As proinflammatory cytokines released during ischaemia are detrimental to the brain, the study aimed to evaluate serum interleukin-18 (IL-18) levels in stroke patients and to investigate the relation between these and epidemiological and clinical data. The study comprised 23 ischaemic stroke patients and 15 controls. Blood sampling for IL-18 determination and for chemistry, and brain CT were performed within 24 h of stroke, while neurological stroke severity and functional disability were estimated, respectively, with the Scandinavian stroke scale (SSS) and Barthel index (BI) within the same interval and two weeks later. There were higher serum IL-18 levels in stroke patients. These correlated with erythrocyte sedimentation rate (ESR), brain CT hypodense area volumes, and SSS and BI scores calculated at both studied times. Moreover, IL-18 levels were higher in patients with non-lacunar stroke subtype than in those with lacunar strokes. The results suggest that IL-18 is involved in stroke-induced inflammation and that initial serum IL-18 levels may be predictive of stroke outcome.

Aged↗
PubMed2002

sPECAM-1 in serum and CSF of acute ischaemic stroke patients.

OBJECTIVES: As platelet endothelial cell adhesion molecule-1 (PECAM-1) is one of key mediators of transendothelial migration of leucocytes during inflammation, and inflammatory reaction is observed in cerebral ischaemia, we decided to determine the levels of soluble PECAM-1 (sPECAM-1) in serum and cerebrospinal fluid (CSF) of patients with acute stroke. MATERIAL AND METHODS: Twenty-three patients with first-ever in a lifetime completed ischaemic stroke have been studied. CSF and blood samples were obtained within 24 h of the onset of stroke and the levels of sPECAM-1 in serum and CSF were quantified by ELISA. RESULTS: Stroke patients displayed statistically significant higher levels of sPECAM-1 in sera and CSF in comparison with control group. The levels were significantly higher in serum than in CSF, correlated between each other, and CSF sPECAM-1 fraction was blood-derived. CONCLUSION: Our results indirectly suggest that PECAM-1 may play a role in the pathophysiological events during early phase of ischaemic stroke.

Aged↗
PubMed2001

Tumour necrosis factor-alpha is increased in the cerebrospinal fluid and serum of ischaemic stroke patients and correlates with the volume of evolving brain infarct.

A growing body of evidence suggests the involvement of inflammatory mediators, including cytokines, in the development of ischaemic brain lesions. The aim of the present study was to investigate whether tumour necrosis factor-alpha (TNF-alpha), the proinflammatory cytokine, contributes to early pathophysiological mechanisms leading to brain damage as a consequence of acute stroke. We have studied TNF-alpha levels in cerebrospinal fluid (CSF) and serum in 23 stroke patients within the first 24 hours after ischaemic stroke, confirmed by computerized tomography of the brain (CT). The control group consisted of 15 patients with the diagnosis of tension headache and neurasthenia. In stroke patients the levels of TNF-alpha both in CSF and serum were significantly higher in comparison with the control group. The positive correlation between the levels of TNF-alpha in CSF and serum of the studied patients has been observed. Furthermore, a positive correlation between both TNF-alpha levels in CSF and serum and the volume of evolving brain infarct have been shown.

Adult↗
PubMed2001

Early TNF-alpha levels correlate with ischaemic stroke severity.

OBJECTIVES: The study aimed to evaluate the levels of an important proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) in cerebrospinal fluid (CSF) and serum in acute stroke and to study the relation between those and the neurological stroke severity and functional disability. MATERIAL AND METHODS: The investigations comprised 23 ischaemic stroke patients. CSF and blood samples were obtained 24 h after the onset of stroke, and stored until analysis. Patients were examined according to Scandinavian Stroke Scale (SSS) and to Barthel Index (BI). RESULTS: The patients displayed statistically significant high levels of TNF-alpha in CSF and sera within the first 24 h of stroke. These correlated significantly with SSS and BI scores calculated within the same interval, and 1 and 2 weeks later. CONCLUSION: Our results suggest the involvement of TNF-alpha in mechanisms of early stroke-induced inflammation and a predictive value of the initial TNF-alpha levels for the outcome of stroke.

Aged↗
PubMed2001

Monocyte chemoattractant protein-1 is increased in the cerebrospinal fluid of patients with ischemic stroke.

BACKGROUND AND PURPOSE: Animal models of stroke have shown that focal cerebral ischemia results in an increased expression of several cytokines and chemokines that precedes leukocyte infiltration into ischemic lesions. The infiltrated leukocytes are thought to contribute to tissue injury in stroke. Monocyte chemoattractant protein-1 (MCP-1) may play an important role in monocyte/macrophage infiltration in stroke patients. METHODS: We studied MCP-1 level in sera and the cerebrospinal fluid of 23 ischemic stroke patients 24 hours after the onset of neurological symptoms and compared the results with 15 control patients with tension headache. The MCP-1 level was determined by ELISA. RESULTS: There was a significant increase of cerebrospinal fluid MCP-1 level in the studied stroke patients in comparison with the control group. The serum level of MCP-1 did not differ from that of control patients. CONCLUSIONS: Our results suggest that MCP-1 may play a role in the inflammatory reaction during the early phase of ischemic stroke.

Aged↗
PubMed2001

The levels of TNF-alpha in cerebrospinal fluid and serum do not correlate with the counts of the white blood cells in acute phase of ischaemic stroke.

Stroke-induced inflammatory reaction, which leads to invasion of leukocytes into the evolving brain infarct, seems to play a key role in the deterioration of brain ischaemic impairment. We have studied CSF and serum levels of tumour necrosis factor-alpha (TNF-alpha), the potent proinflammatory cytokine, and peripheral white blood cells (WBC) counts in patients within the first 24 hours of ischaemic stroke. TNF-alpha levels in CSF and serum as well as WBC counts were increased. There was no correlation between TNF-alpha levels either in CSF and serum or in WBC counts. The results of our study suggest that increased CSF TNF-alpha levels may represent acute intracerebral inflammation in stroke, whereas elevated levels of TNF-alpha in serum may reflect the peripheral proinflammatory state as well as stroke-induced systemic inflammatory reaction. Increased CSF and serum TNF-alpha levels do not correlate with the elevation of WBC counts, suggesting that TNF-alpha overexpression observed in early phase of stroke is not dependent on increased total number of peripheral leukocytes.

Acute Disease↗
PubMed2000

Contribution of tumor necrosis factor alpha to the pathogenesis of stroke.

Tumor necrosis factor alpha (TNF-alpha) is a protein of a cellular origin belonging to a group of proinflammatory cytokines. A rapid overproduction of TNF-alpha in a cerebral post-ischemic inflammatory response leads to the stimulation of adhesive molecules expression with subsequent accumulation of leukocytes in the ischemic focus, which is preceded by their adhesion and migration. The TNF-alpha proinflammatory activity results mainly in extending the area of the brain infarct, which brings about negative clinical implications. Being the final morphological effect of ischemic stroke, TNF-alpha appears also to contribute to neuronal necrosis by its involvement in the process of apoptosis as well as in the death of neurons. The present study describes and discusses mainly the contribution of TNF-alpha to the formation of ischemic focus in the brain.

Animals↗
PubMed1998

Intrafamilial variability of the ocular phenotype in a Polish family with a missense mutation (A63D) in the Norrie disease gene.

PURPOSE: To describe the phenotypic variability in a Polish Norrie disease (ND) family associated with the missense mutation A63D. METHODS: A patient with spared vision from a Polish ND family underwent detailed ophthalmological examinations including slit-lamp biomicroscopy, ultrasound (USG), angiography, Goldmann kinetic visual field, and electroretinography (ERG). Mutation screening was carried out using the single-strand conformation polymorphism (SSCP) technique and subsequent DNA sequencing of the coding part of the ND gene. RESULTS: A mutation was detected (exon 3, A63D) in a large Polish family with 12 affected males, all but one presenting with classical ND symptoms. In one male, partially preserved vision was observed up to 40 years of age (distance acuity of the right eye 1/50 and left eye 2/50). Slit-lamp examination revealed remnants of a persistent primary vitreous and hyaloid artery. Upon angiography, the retina was vascularized within the posterior pole but not in the periphery. The ERG revealed pathological changes characteristic for chorioretinal degenerations. CONCLUSION: Within one family, individuals with identical sequence alterations in the ND gene can show remarkable phenotypic variability of the ocular symptoms. These findings indicate the involvement of additional factors (epigenetic or genetic) in ocular pathogenesis of ND.

Adult↗
PubMed1998

[Use of pleuro-peritoneal shunt in the treatment of chronic chylothorax].

Persistent chylothorax is usually treated by frequent aspirations or intercostal-tube drainage with interpleural installation of chemical or mechanical irritants. In 1986 Denver pleuroperitoneal shunt has been introduced. This is a single-unit silicone rubber conduit consisting of unidirectional valved pumping chamber located between pleural and peritoneal catheters. Manual compression of the shunt is required to achieve active pumping. The described unit is implanted subcutaneously in the lover thoracic and upper abdominal region in the anterior axillary line. We present a 38 year old patient with persistent chylothorax treated successfully by implantation of the described device.

Adult↗
PubMed1998

[Open neural tube defects in prenatal diagnosis].

The problem of open neural tube defects (ontd) is discussed in the light of results of prenatal tests performed in the district of Warsaw. These results seem to bear some epidemiological significance allowing estimation of approximate frequency of ontd as well as recurrence risk for the purpose of genetic counselling. Prenatal diagnosis of ontd is very important for individual families--particularly those with increased risk. However, in view of very small number of prenatal tests and the fact that maternal serum screening and ultrasonografic screening are practically not available the demographic impact of prenatal diagnosis in Poland on the frequency of ontd (and other genetic diseases) in Poland must be negligible.

Acetylcholinesterase↗
PubMed1997

Two distinct deletions in the IDS gene and the gene W: a novel type of mutation associated with the Hunter syndrome.

A novel mutation has been identified in a patient with the Hunter syndrome (mucopolysaccharidosis type II), in whom the disorder is associated with two distinct deletions separated by 30 kb. The deletions were characterized by Southern blot and PCR analyses, and the nucleotide sequences at both junctions were determined. The first deletion, corresponding to a loss of 3152 bp of DNA, included exons 5 and 6 of the iduronate-2-sulfatase (IDS) gene. The second deletion was 3603 bp long and included exons 3 and 4 of gene W, which is located in the DXS466 locus telomeric of the IDS gene. Both deletions are the result of nonhomologous (illegitimate) recombination events between short direct repeats at the deletion breakpoints. An interesting finding was the presence of the heptamer sequence 5'-TACTCTA-3' present at both deletion junctions, suggesting that this motif might be a hot spot for recombination. We propose that the double deletion is the result of homology-associated nonhomologous recombinations caused by the presence of large duplicated regions in Xq27.3-q28.

Base Sequence↗
PubMed1997

Identification of 16 sulfamidase gene mutations including the common R74C in patients with mucopolysaccharidosis type IIIA (Sanfilippo A).

Mucopolysaccharidosis type IIIA (MPS IIIA or Sanfilippo A disease) is a storage disorder caused by deficiency of the lysosomal enzyme sulfamidase. Mutation screening, using SSCP/heteroduplex analyses on cDNA and genomic DNA fragments, was performed in a group of 42 European patients. Sixteen of the 17 different gene mutations characterized have not been previously described. The spectrum of gene lesions consists of two 1-bp deletions (1091delC, 1093delG), an 18-bp duplication (421ins18), a splice site mutation (IVS2-2A-->G), and 13 different missense point mutations. As in other lysosomal storage disorders, the phenotypic heterogeneity is associated with a considerable genetic heterogeneity. The missense mutation R74C, which alters an evolutionary conserved amino acid in the active site of the enzyme, was found on 56% of alleles of 16 Polish patients, whereas it was less frequent among German patients (21% of disease alleles). R245H, a previously reported common mutation, represents 35% of disease alleles in German patients, but only 3% in Polish patients. As the combined frequency of the common mutations (R74C and R245H) in German and Polish populations exceeds 55%, screening for these two mutations will assist molecular genetic diagnosis of MPS IIIA and allow heterozygote testing in these populations.

Binding Sites↗