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Biomedical subjects

Anna Członkowska

Publications and source records attributed to Anna Członkowska.

At least 19 recordsLinked to original sources
PubMed2006

Acute ischemic stroke care and outcome in centers participating in the Polish National Stroke Prevention and Treatment Registry.

BACKGROUND AND PURPOSE: Significant intercenter variability in quality of care and stroke outcomes was found in many countries. The aim of the study was to compare the acute ischemic stroke care and outcomes in centers participating in the Polish National Stroke Prevention and Treatment Registry. METHODS: The World Health Organization Stepwise Approach to Stroke Surveillance-based questionnaire was used to collect data on patients admitted to participating centers between December 1, 2001, and July 31, 2002. To ensure data quality, only centers reporting representative sample of patients were analyzed. Ischemic stroke patient characteristics, in-hospital care, and early outcomes (adjusted for case mix) were compared for participating centers. RESULTS: There were 26 of 48 centers that met inclusion criteria, with a total of 8736 patients (52% women; mean age 71 years, with a range among institutions from 68 to 75 years). Significant differences between centers were observed for distribution of risk factors and in-hospital care. The rates for death and poor outcome (defined as a Rankin score > or =3 or death) ranged from 8.0% to 31.8% and from 44.2% to 74.7%, respectively. After adjusting for case mix, the death or poor outcome prognoses remained significantly different between centers. CONCLUSIONS: The observed significant differences between Polish stroke centers indicate the need for improvement of patient education, effective stroke risk factor control, and standardized in-hospital care.

Acute Disease↗
PubMed2006

p.H1069Q mutation in ATP7B and biochemical parameters of copper metabolism and clinical manifestation of Wilson's disease.

We compared the effect of the p.H1069Q mutation and other non-p.H1069Q mutations in ATP7B on the phenotypic expression of Wilson's disease (WD), and assessed whether the clinical phenotype of WD in compound heterozygotes depends on the type of mutation coexisting with the p.H1069Q. One hundred forty-two patients with clinically, biochemically, and genetically diagnosed WD were studied. The mutational analysis of ATP7B was performed by direct sequencing. A total number of 26 mutations in ATP7B were identified. The p.His1069Gln was the most common mutation (allelic frequency: 72%). Seventy-three patients were homozygous for this mutation. Of compound heterozygotes, 37 had frameshift/nonsense mutation, and 20 had other missense mutation on one of their ATP7B alleles. Twelve patients had two non-p.H1069Q mutations. Patients homozygous for the p.H1069Q mutation had the less severe disturbances of copper metabolism and the latest presentation of first WD symptoms. The most severely disturbed copper metabolism and the earliest age at initial disease manifestation was noticed in non-p.H1069Q patients. In compound heterozygotes, the type of mutation coexisting with the p.H1069Q to a small extent influenced WD phenotype. The phenotype of WD varied considerably among patients with the same genotype. The p.H1069Q mutation is associated with late WD manifestation and with a mild disruption of copper metabolism. In compound heterozygotes, the phenotype of WD to a small extent depends on the type of mutation coexisting with the p.H1069Q. Besides genotype, additional modifying factors seem to determine WD manifestations.

Adenosine Triphosphatases↗
PubMed2006

Gender differences in neurological disease: role of estrogens and cytokines.

Increasing evidence suggests that inflammatory response may be a critical component of different brain pathologies. However, the role played by this reaction is not fully understood. The present findings suggest that neuroinflammtory mediators such as cytokines may be involved in a number of key steps in the pathological cascade of events leading to neuronal injury. This hypothesis is strongly supported by experimental and clinical observations indicating that inhibition of the inflammatory reaction correlates with less neuronal damage. Estrogens are thought to play a role in the sex difference observed in many neurological diseases with inflammatory components including stroke, Alzheimer's and Parkinson's diseases, multiple sclerosis, or amyotrophic lateral sclerosis. Clinical and experimental studies have established estrogen as a neuroprotective hormone in these diseases. However, the exact mechanisms involved in the neuroprotective effects of estrogens are still unclear. It is possible that the beneficial effects of these hormones may be dependent on their inhibitory activity on the inflammatory reaction associated with the above-mentioned brain pathologies. Here, we review the current clinical and experimental evidence with respect to the inflammation-modulating effects of estrogens as one potential explanatory factor for sexual dimorzphism in the prevalence of numerous neurological diseases.

Animals↗
PubMed2006

Ultrastructural picture of blood vessels in muscle and skin biopsy in CADASIL.

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy) is an inherited systemic vascular disorder affecting mainly the central nervous system. We performed detailed ultrastructural examination of the small vessels in the skin and skeletal muscle of a 51-year-old patient with bilateral cerebral white matter lesions, who had a history of two ischaemic strokes. The arterioles were characterized by degeneration and loss of vascular smooth muscle cells (VSMCs). GOM deposits, varied in size and shape, were located in the neighbourhood of the smooth muscle cells, often within an infolding of the cell membrane. No apparent correlations between presence, size or number of GOM deposits and damage severity of vascular smooth muscle cells were seen. Moreover, in some capillaries there were GOM deposits which were seen in the basement membrane near pericytes and endothelial cells. On the other hand, lesions of VMSCs and/or endothelial cells were also visible on the sections of blood vessels devoid of GOM deposits. Genetic tests detected a mutation in exon 4 of the Notch3 gene. It confirmed the initial diagnosis which had been suggested on the basis of the clinical and MRI findings.

Biopsy↗
PubMed2005

APOE genotype and serum cholesterol in predicting risk for early death from ischemic stroke in men and women.

BACKGROUND: We recently discovered that APOE epsilon3/epsilon4 genotype in men and APOE epsilon2/epsilon3 genotype in women are associated with increased risk of death from ischemic stroke (IS). One of the main physiological roles of apolipoprotein E is participation in cholesterol metabolism. A significant association of low serum cholesterol level with increased risk of death from stroke was documented. So, we aimed to establish if an association exists between APOE genotype, serum cholesterol and 1-month mortality in IS. METHODS: We studied 666 patients (330 men, 336 women) with a diagnosis of IS. Total serum cholesterol (TC) was measured with the method of Abbott Spectrum (USA). APOE genotyping was performed by PCR-RFLP method. RESULTS: The highest frequency of low serum TC was associated with APOE epsilon2/epsilon3 genotype (both in men and in women). Low serum TC was associated with increased mortality rate only in women; this effect was evident only in females not possessing APOE epsilon2/epsilon3. Female patients with APOE epsilon2/epsilon3 genotype had high 1-month mortality rate independently from serum TC. In multiple regression analyses APOE epsilon3/epsilon4 genotype in men and APOE epsilon2/epsilon3 genotype in women predicted risk of death independently from serum TC and also from other potential pre- and post-stroke prognostic factors. CONCLUSION: APOE epsilon3/epsilon4 genotype in men and APOE epsilon2/epsilon3 in women are associated with increased 30-day mortality in stroke. This effect seems be independent from serum cholesterol.

Aged↗
PubMed2004

Influence of gender on baseline features and clinical outcomes among 17,370 patients with confirmed ischaemic stroke in the international stroke trial.

AIM: We sought to determine whether there were differences between men and women with acute stroke in their baseline characteristics and outcome in a large cohort of patients randomized in the International Stroke Trial (IST). METHODS: Of the 19,435 patients randomized in the IST, 17,370 had an ischemic stroke confirmed by CT scan or autopsy (8,003 female and 9,367 male). In males and females, we compared baseline characteristics (age, frequency of atrial fibrillation, pre-stroke administration of aspirin and systolic blood pressure, conscious level, stroke syndrome) and outcome at 14 days and 6 months (death, complications, dependency, recovery, place of residence). We developed a specific logistic regression model to adjust for case-mix in order to evaluate the separate influence of gender on outcome. RESULTS: Female patients were older, suffered more frequently from atrial fibrillation, had higher systolic blood pressure at randomization and generally had more severe strokes (a higher proportion were unconscious or drowsy or had a total anterior circulation syndrome). Females had higher 14-day and 6-month case fatality and were more likely to be dead or dependent at six months (and consequently more likely to require institutional or residential care). Gender was an independent predictor of death or dependency at 6 months. CONCLUSIONS: The adverse effect of female gender on outcome indicates that further research to explore the underlying biological mechanism is justified, and that more intensive acute and long-term treatment may be needed to improve outcome among female patients with stroke.

Acute Disease↗
PubMed2004

Cyclooxygenases mRNA and protein expression in striata in the experimental mouse model of Parkinson's disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration to mouse.

Cyclooxygenases (COX) are associated with complex alteration in many pathologies of the central nervous system (CNS). Increased expression of COX-2 has been shown in injured or degenerated neurons, thus suggesting that COX-2 may contribute to neuronal damage. In this study, we present the expression of COX-1 and COX-2 mRNA and protein in striatum following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to mice. MPTP causes an acute damage of dopaminergic neurons especially in the nigrostriatal dopaminergic system, thus diminishing dopamine (DA) content in striatum and decreasing the number of dopaminergic cells in the pars compacta of the substantia nigra (SN). C57Bl mice have received 60 mg/kg of MPTP introperitoneally. A group of mice received also rofecoxib 10 mg/kg from the 1st day following MPTP administration. Dopamine content in striatum (high-performance liquid chromatography-HPLC), mRNA expression of COX-1 and -2 (reverse transcriptase-polymerase chain reaction technique-RT-PCR), COX-1 and -2 protein content (immunoblotting) have been measured on day 1st, 3rd, 7th, 14th and 21st after the injury. We have found that COX-1 mRNA expression is not changed following MPTP administration, but COX-2 gene and protein expression in striatum increases from the 3rd to the 7th and 14th days, and diminishes on the 21st day. Production of prostaglandins is augmented only briefly after MPTP treatment and did not correlate with increased COX-2 mRNA and COX-2 protein production. Thus, the increase of COX-2 expression does not follow the acute stage of cell death but rather the recovery period after the injury. We also demonstrate that COX-2 activity inhibition by rofecoxib (10 mg/kg), which has been started 1 day after the injury, has not neuroprotective effect. Our study suggests that COX-2 does not contribute to neurons death following MPTP administration and that the inhibition of COX-2 activity is not beneficial to neurons injured by MPTP. However, COX-2 mRNA and protein expressions increase after MPTP injury; the role of these findings remains obscure.

Animals↗
PubMed2004

Dexamethasone protects against dopaminergic neurons damage in a mouse model of Parkinson's disease.

The pathological process of neurodegeneration, which is observed in Alzheimer's (AD) and Parkinson's (PD) diseases and that follows any insult to the central nervous system, is accompanied by an inflammatory reaction, which is believed to contribute to the pathogenesis of the diseases. In accordance to this, the anti-inflammatory agents are suggested to be effective in slowing or inhibiting the degenerative process. In this study, we investigated the influence of dexamethasone (DXM) on the nigrostriatal dopaminergic neurons damage following administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP). Mice C57BL received pre-treatment of the various doses of dexamethasone followed by MPTP administration (40 mg/kg). We found that dexamethasone 1 mg/kg diminished a dopamine content depletion in striatum by about 20%, when the doses of 0.1 mg/kg was ineffective and 10 mg/kg even aggravate the dopamine content decrease. In the second step of the experiment, we chose the effective doses, 1 mg/kg, and started the treatment before and 24 h after MPTP administration. We observed the same protection in both situations: less dopamine depletion and less decrease in the number of dopaminergic cells in the substantia nigra (SN). Dexamethasone also similarly decreased the inflammatory reaction (glial activation, lymphocytic infiltration) in the injured areas. Our study showed that dexamethasone may exert a neuroprotective effect towards neurons injured by MPTP, but only when used in a proper dose. The mechanism of dexamethasone protective properties may be an inhibition of inflammatory process; however, direct interactions with neurons are also possible.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

Agreement between the clinical Oxfordshire Community Stroke Project classification and CT findings in Poland.

The Oxfordshire Community Stroke Project (OCSP) classification provides a simple means of classifying the clinical syndromes associated with acute stroke. The validity of the classification can depend on many factors. Accuracy and time of the clinical and radiological examination are very important. It was used in the International Stroke Trial (IST). The study was conducted in 467 hospitals in 34 countries. Our aim was to assess how well the OCSP classification could predict infarct site and size on computed tomography (CT) scan when performed in a trial within 48 h after the onset of stroke and the clinical assessment was carried out by different doctors in different hospitals. We examined data on the patients randomized in the IST by the seven participating hospitals in Poland. Patients admitted to the hospital were examined by the doctor on duty. Eight aspects of the neurological deficit present just before randomization were recorded. The computer system in the randomization centre employed a validated algorithm to assign the patient to one of the four infarct syndromes: lacunar syndrome (LACS), partial anterior circulation syndrome (PACS), total anterior circulation syndrome (TACS) and posterior circulation syndrome (POCS). We assessed the localization and extent of the recent infarction on available CT scans and correlated these with the computer-assigned OCSP category. CT scans were available for 558/759 (74%) of the patients randomized in Poland. In 458 (82%) of cases, CT was carried out in the first 24 h after the onset of stroke. In 444 (80%) scans, a recent infarct was visible. These radiological lesions were appropriate to the clinical classification in 56% of patients with TACS, 73% with PACS, 61% with LACS and 59% with POCS. In Polish centres in IST, amongst the patients with infarction visible on CT, the OCSP subtype predicted the size and site of the infarct in about two-thirds of cases. These data suggest that, provided its limitations are taken into account, the classification can be usefully applied in multicentre clinical trials (or epidemiological studies) and to aspects of the routine clinical care of patients with acute stroke.

Aged↗
PubMed2003

Changes of percentages in immune cells phenotypes and cytokines production during two-year IFN-beta-1a treatment in multiple sclerosis patients.

OBJECTIVE: The aim of the study was to find out whether INF-beta-1a influences the immune profile of peripheral blood (PB) leukocytes in MS patients. METHOD: We have studied 20 patients with relapsing-remitting form of MS treated with INF-beta-1a using twocolor cytometry. We determined immune cells phenotypes and production of some cytokines: IL-4, IL-10, IL-12, IFN-gamma, before drug administration and after starting the treatment. RESULTS: In MS patients an increased percentage of CD14(+)CD86(+) cells and CD3(+)CD25(+) cells was noticed after 6, 9 and 12 months of INF-beta-1a therapy. Among cytokine-producing cells we noted an increased fraction of CD3(+)IL-4, CD14(+)IL-10 and CD14(+)IL-12 cells after 12 months, which decreased to the level observed before treatment after 24-month therapy. CONCLUSIONS: IFN-beta-1a treatment was associated with significant changes in immune response. This effect was mostly evident within the first year of treatment.

Adjuvants, Immunologic↗
PubMed2003

Self-rated emotional functioning of patients with neurological or asymptomatic form of Wilson's disease.

Psychopathology was assessed in 50 patients with the neurological form of Wilson's disease (WD-N) and in 17 asymptomatic patients (WD-A) compared to matched healthy controls and to rheumatoid arthritis (RA) control patients using The Hopkins Symptom Checklist. As hypothesized, WD-N patients had significantly lower interpersonal sensitivity and aggression/hostility scores than had healthy controls, but did not differ from them either in depression or anxiety levels. Retarded depression and anxiety were higher among RA patients than in WD-N patients. This nondistressed response to the chronic disabling disease was even more salient in 19 WD patients with lesions in basal ganglia only. WD-A patients did not differ from their healthy peers, which suggests a tendency towards hypercompensation and denial in the former. WD-N patients' limited awareness of their deficits (including impaired control of affective behavior) seems to result from their brain damage implicating the basal ganglia.

Adolescent↗
PubMed2003

The polish experience in early stroke care.

Stroke units are being organised in Poland since 1997. To ensure easy access to stroke care, 120 specialised units need to be created. There were 23 stroke units in Poland in the year 2000. Only 12 of them fulfilled the criteria of a standard stroke unit. Significant differences in stroke fatality were noted between well- and as yet insufficiently organised units. These results indicate a need for monitoring the implementation of the basic standards in stroke units.

Brain Ischemia↗
PubMed2003

Dynamics of expression of the mRNA for cytokines and inducible nitric synthase in a murine model of the Parkinson's disease.

The inflammatory reaction and oxidative stress has been linked with PD. Proinflammatory cytokines promote neurodegeneration or neuroprotection in different animal models. In addition, these cytokines have been reported to increase iNOS expression. With the RT-PCR method we evaluated mRNA levels for IL 1beta, IL6, TNF, IFNgamma, IL-10 and iNOS in the striatum of C57BL/6 mice after MPTP intoxication. The IL1beta mRNA expression rapidly increased and peaked at 6 h. The first increase of mRNA for TNFalpha and IFNgamma was noticed at 6-24 h and the second at the 7th day after MPTP intoxication. Two peaks of IL10 mRNA were seen, immediately (6 h) and at the 3 day post MPTP injection. The peak of mRNA level for IL6 was observed at the 7th day. Expression of mRNA for iNOS peaked at 24 h, started decreasing on the 3rd day, but was still present till the 14th day. Those findings suggest that cytokine network and iNOS may be involved in the development of immune changes accompanying degeneration of the nigrostriatal system.

Animals↗
PubMed2003

Concomitant heterozygous factor V Leiden mutation and homozygous prothrombin gene variant (G20210A) in patient with cerebral venous thrombosis.

BACKGROUND: Factor V Leiden mutation represents the most common genetic risk factor of venous thrombosis in Caucasian population. A common mutation in prothrombin gene, which is due to G-->A transition at position 20210, is also associated with elevated prothrombin concentration and thrombosis. Both this mutations may constitute concomitant risk factors for deep venous thrombosis. CASE REPORT: A 29-years old woman was admitted in the Emergency Department because of severe headache with vomiting that she suffered for a few days without any neurological deficits. In the Emergency she presented first in her life tonic-clonic seizures followed by right hemiparesis and aphasia and than was admitted to hospital. CT and MR scan showed a large lesion in the left fronto-parietal region with extent edema, which was first diagnosed as tumor. Following MR showed more lesions and typical signs of sinus thrombosis. She improved quickly after stroke without any anticoagulant treatment. Genetic study revealed factor V Leiden mutation and homozygous mutation G20210A in prothrombin gene. CONCLUSIONS: Both mutations found in this case, alone, are not a high risk factors for venous thrombosis but together may increase 5-10 fold risk of venous thrombosis. Venous stroke must be considered always in acute neurological events with organic brain lesions, especially in young

Adult↗
PubMed2003

Influence of estrogens on neurodegenerative processes.

Gonadal steroids are known to be of prime importance in the normal maintenance of brain function. Data from epidemiological studies suggest that the decline in estrogen following menopause may increase the risk of neurodegenerative diseases. There is accumulating epidemiological evidence for neuroprotection by estrogens against neurodegenerative diseases, such as Alzheimer's disease. Although it is unclear whether estrogen may be effective in preventing further cognitive decline in women who already have Alzheimer's disease, several studies indicate that estrogen replacement improves the cognitive performance of postmenopausal women. Despite the somewhat controversial data from human studies, experimental investigations in different animals have shown that estrogen is neuroprotective. Although estrogens are known to exert several direct effects on neurons, the cellular mechanisms involved in the neuroprotective effects of estrogen are still unclear. Estrogen causes most of its neuroprotective effects by means of direct binding to specific nuclear receptors. The anti-oxidant effects of estrogens and activation of different membrane-associated intracellular signaling pathways or neurotrophic cross talk through the signal cascade shared with neurotrophic factors could also contribute to neuroprotection. In this article, we outline the evidence supporting a direct role of estrogen in neuronal survival, and

Antioxidants↗
PubMed2003

[Does gender exert influence on stroke?].

Stroke morbidity increases with age. That is the reason why it affects especially the middle aged and elderly. Life expectancy is longer for females than males by 10 years, that is why stroke is a major problem in women. Women die twice more frequently from stroke than men (16% vs. 8%). Stroke risk factors are basically the same in spite of gender. The most important are hypertension, diabetes, dyslipidaemia, atrial fibrillation, coronary heart disease, previous stroke, smoking, alcohol abuse, obesity and lack of physical activity. Their impact, however, is different in males and females. Women with diabetes, atrial fibrillation, myocardial infarction, obese, drinking excessive amounts of alcohol and smoking are more likely to suffer of stroke than males with the same burden. A less favourable outcome after stroke has been observed in female patients--higher mortality rates and disability. It is possible that poor prognosis is related to a drop in blood estrogen concentration after menopause. Estrogen replacement therapy has not proved to be beneficial in preventing stroke and improving outcome. There are several specific conditions: pregnancy, migraine in women associated with the occurrence of stroke.

Adult↗
PubMed2002

High early case fatality after ischaemic stroke in Poland: exploration of possible explanations in the International Stroke Trial.

PURPOSE: To determine why Polish patients included in the International Stroke Trial (IST) had a higher early case fatality than patients from other countries. METHODS: Of 19,435 patients randomised to IST, 17,370 had CT or autopsy-confirmed ischaemic stroke. We compared the baseline clinical state and 14-day case fatality of patients randomised in Polish centres with those from all other IST countries. We examined: age, gender, presence of atrial fibrillation (AF), conscious level, neurological deficit, cause of death and aspirin use in the 3 days before stroke. RESULTS: In Poland, the 14-day case fatality rate was significantly higher than in other IST countries (13% vs. 9.6%; odds ratio, OR, 1.5, 95% confidence interval, CI, 1.2-1.9). In Poland, a significantly higher proportion of deaths was attributed to coronary heart disease (2.5% vs. 0.7%) and pulmonary embolism (1.0% vs. 0.4%). Polish patients had higher percentage of AF and drowsiness, but were younger. When these factors were adjusted for, Polish patients still had approximately a 57% higher risk of death within 14 days compared with other countries. A logistic regression analysis revealed that an increased risk of death within 14 days in Poland compared to other IST patients was present among patients younger than 75 years (OR 1.7; 95% CI 1.3-2.4), females (OR 1.8; 95% CI 1.3-2.5), patients who were alert at onset (OR 2.4; 95% CI 1.7-3.4), with partial anterior circulation syndrome (PACS) (OR 2.0; 95% CI 1.4-2.8) or lacunar syndrome (LACS) (OR 2.4; 95% CI 1.1-5.0) and without AF (OR 1.8; 95% CI 1.3-2.4). Polish patients were less likely to have been on aspirin before their stroke than other countries (7.6% vs. 20.8%). CONCLUSION: The 14-day case fatality was significantly higher in Poland than in other countries in IST. Part of the increase was due to greater stroke severity in the Polish patients. However, differences persisted even after adjustment for baseline stroke severity. Several factors may have contributed the excess: poor attention to treatment of cardiovascular disease, less attention to treatment of secondary complications of stroke and some other--as yet unidentified--factor specific to Poland.

Age Factors↗