[Evaluation of the prevalence and determinants of shift work sleep disorders]. / Ocena rozpowszechnienia i uwarunkowan zaburzen snu u pracowników zmianowych.

BACKGROUND: Nowadays, shift work is a necessity. Unfortunately, according to many studies, it carries serious health implications, e.g. sleep disorders. OBJECTIVE: To assess the prevalence and determinants of sleep disorders among shift workers compared with daytime workers. MATERIALS AND METHODS: The study was conducted with use of a questionnaire, containing Sleep Quality Scale (SQS) and Epworth Sleepiness Scale (ESS) to assess sleep quality, as well as a set of open and closed questions concerning the factors that may interfere with sleep. RESULTS: Data have been collected from 286 individuals; 52.8% of shift workers (case group) and 47.2% of regular daytime workers (control group). There was a significant difference in the quality (SQS) of sleep (31.3 +/- 6.50 vs. 27.6 +/- 5.49) and the evaluation (ESS) of sleepiness (8.4 +/- 3.85 vs. 7.6 +/- 4.04) between the two groups. No significant correlations were found between the ESS and SQS values and reported sleep duration, age of respondents, marital status and napping on the job. The more the night shifts a month, the worse the respondents' quality of sleep (SQS). The employees pointed to irritability, depression, fatigue, emotional tension, impaired family and social life as a result of shift work. CONCLUSIONS: The prevalence of sleep disorders in the entire study population was high, with its considerably higher rate in the group of shift workers. Shift work causes disorders and emotional problems in family life noticeable by the subjects. It would be advisable to carry out training programs addressed to employees and managers in the field of sleep hygiene and activities that minimize the negative consequences of shift work.

Protective effect of intermittent clamping of the portal triad in the rat liver on liver ischemia-reperfusion injury.

BACKGROUND: Intermittent clamping (IC) of the portal triad is an effective method of protecting the liver from ischemia-reperfusion injury (IR). In clinical practice, this method is employed during a resection, but its mechanism is still not clear. OBJECTIVES: To evaluate the effect of IC on rat liver and determine its mechanisms. MATERIALS AND METHODS: Wistar rats were submitted to 60-min IC (cycles of 12-min clamping followed by 4-min reperfusion), and the samples were collected after 1, 6, and 72 hrs of reperfusion. We determined the serum activity of alanine aminotransferase (ALT), and measured the concentration of TNF-α, malondialdehyde (MDA) and myeloperoxidase (MPO) in liver homogenates. The apoptosis of hepatocytes was evaluated immunohistochemically. RESULTS: When compared to the IR rats, the activity of ALT decreased in the IC group in all periods of observation (the highest decrease of ~48% after 1 hr of reperfusion). When compared to the IR group, a statistically significant decrease (p < 0.05) in the TNF-α concentration (~33%) in the IC rats occurred only after 1 hr of reperfusion, and it was accompanied by a decrease in the MPO concentration after 1 and 6 hrs of reperfusion. IC reduces the effects of reactive oxygen species (ROS) activity, which has been confirmed by a statistically significant decrease in MDA concentration by 25%-35% in all studied periods. The limitation of hepatocytes apoptosis due to IC occurs in the early (~26%; p < 0.05) and late (~45%; p < 0.01) phases of reperfusion. CONCLUSIONS: The use of IC in early phase of reperfusion brings about a decrease in TNF-α release, which can be related to liver injury due to neutrophil infiltration and apoptotic cell reduction. It seems that the reduction of lipid peroxidation may also limit the liver injury.

Ontogenetic serotoninergic lesioning alters histaminergic activity in rats in adulthood.

The aim of this study was to determine histamine content in the brain and the effect of histamine receptor antagonists on behavior of adult rats lesioned as neonates with the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). At 3 days after birth Wistar rats were pretreated with desipramine (20 mg/kg ip) before bilateral icv administration of 5,7-DHT (37.5 µg base on each side) or saline-ascorbic (0.1%) vehicle (control). At 10 week levels of 5-HT and its metabolite 5-hydroxyindole acetic acid (5-HIAA) were determined in frontal cortex, striatum, and hippocampus by an HPLC/ED technique. In the hypothalamus, frontal cortex, hippocampus and medulla oblongata, the level of histamine was analyzed by an immunoenzymatic method. Behavioral observations (locomotion, exploratory-, oral-, and stereotyped activity) were performed, and effects of DA receptor agonists (SKF 38393, apomorphine) and histamine receptor antagonists S(+)chlorpheniramine (H(1)), cimetidine (H(2)), and thioperamide (H(3)) were determined. We confirmed that 5,7-DHT profoundly reduced contents of 5-HT and 5-HIAA in the brain in adulthood. Histamine content was also reduced in all examined brain regions. Moreover, in 5,7-DHT-lesioned rats the locomotor and oral activity responses to thioperamide were altered, and apomorphine-induced stereotype was intensified. From the above, we conclude that an intact central serotoninergic system modulates histamine H(3) receptor antagonist effects on the dopaminergic neurons in rats.

Thioperamide, an H3 receptor antagonist prevents [³H]glucose uptake in brain of adult rats lesioned as neonates with 5,7-dihydroxytryptamine.

As a first attempt at exploring an association between histaminergic and serotoninergic neuronal phenotypes in glucose regulation, the influence of the histamine H3 receptor antagonist thioperamide on glucose uptake by brain was determined in rats in which the serotoninergic innervations of brain was largely destroyed perinatally. Male Wistar rats were initially treated on the 3rd day after birth with the serotoninergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) (75 µg icv) or saline vehicle (10 µl icv). At 8 weeks lesioned and control rats were terminated in order to validate the effectiveness of 5,7-DHT: reduction in 5-HT and 5-HIAA by 83-91% and 69-83% in striatum, frontal cortex, and hippocampus (HPLC/ED method). Other groups of rats were pretreated with thioperamide (5.0 mg/kg ip) or saline vehicle 60 min prior to 6-[³H]-D-glucose (500 µCi/kg ip). Fifteen-min later rats were decapitated and brains were excised and dissected to remove frontal cortex, striatum, hippocampus, thalamus/hypothalamus, pons, and cerebellum. Liquid scintillation spectroscopy was used to determine that [³H]glucose uptake, which was enhanced in 5,7-DHT lesioned rats in cortex (by 88%), hippocampus, thalamus/hypothalamus, pons and cerebellum (each by 47-56%), and in striatum (by 35%). In contrast, thioperamide prevented the enhancement in [³H]glucose uptake in all brain regions of 5,7-DHT neonatally lesioned rats; and [³H]glucose levels were significantly different in all brain regions (except thalamus/hypothalamus) in thioperamide-versus saline-treated rats. These findings indicate a functional association between histaminergic and serotoninergic systems in brain in relation to glucose regulation.

Ontogenetic exposure of rats to pre- and post-natal manganese enhances behavioral impairments produced by perinatal 6-hydroxydopamine.

Rats lesioned shortly after birth with 6-hydroxydopamine (6-OHDA; 134 µg icv) represent a near-ideal model of severe Parkinson's disease because of the near-total destruction of nigrostriatal dopaminergic fibers. The element manganese, an essential cofactor for many enzymatic reactions, itself in toxic amount, replicates some clinical features similar to those of Parkinson's disease. The aim of this study was to examine the effect of neonatal manganese exposure on 6-OHDA modeling of Parkinson's disease in rats. Manganese (MnCl(2)·4H(2)O) 10,000 ppm was included in the drinking water of pregnant Wistar rats from the time of conception until the 21st day after delivery, the age when neonatal rats were weaned. Control rats consumed tap water. Other groups of neonatal rat pups, on the 3rd day after birth, were pretreated with desipramine (20 mg/kg ip 1 h) prior to bilateral icv administration of 6-OHDA (30, 60, or 137 µg) or its vehicle saline-ascorbic (0.1%) (control). At 2 months after birth, in rats lesioned with 30, 60, or 134 µg 6-OHDA, endogenous striatal dopamine (DA) content was reduced, respectively, by 66, 92, and 98% (HPLC/ED), while co-exposure of these groups to perinatal manganese did not magnify the DA depletion. However, there was prominent enhancement of DA D(1) agonist (i.e., SKF 38393)-induced oral activity in the group of rats exposed perinatally to manganese and also treated neonatally with the 30 mg/kg dose of 6-OHDA. The 30 mg/kg 6-OHDA group, demonstrating cataleptogenic responses to SCH 23390 (0.5 mg/kg) and haloperidol (0.5 mg/kg ip), developed resistance if co-exposed to perinatal manganese. In the group exposed to manganese and lesioned with the 60 mg/kg dose of 6-OHDA, there was a reduction in D(2) agonist (i.e., quinpirole, 0.1 mg/kg)-induced yawning. The series of findings demonstrate that ontogenetic exposure to manganese results in an enhancement of behavioral toxicity to a moderate dose of 6-OHDA, despite the fact that there is no enhanced depletion of striatal DA depletion by the manganese treatment.

[Occupational satisfaction and quality of life in women aged 45-60 years in the Silesia voivodeship]. / Satysfakcja z pracy zawodowej a jakosc zycia kobiet w wieku 45-60 lat w województwie slaskim.

BACKGROUND: Quality of life is an important issue of public health. It becomes essential in the population of active workers, especially women who besides their occupational activity have to perform other important roles, such as care of their children or older parents. MATERIALS AND METHODS: The presented study is an attempt to answer the question on whether occupational activity, especially job satisfaction, provides better quality of live in the population of women aged 45-60 years. RESULTS: The obtained results confirm that a better quality of live, measured by the status of physical and mental health, is characteristic of occupationally active women with a higher level of education, who also experience job satisfaction. Care of children or older parents has no impact on the decline of quality of life. CONCLUSIONS: The improvement of qualifications and occupational activity can contribute to a better quality of live in the population of women.

Neonatal co-lesion by DSP-4 and 5,7-DHT produces adulthood behavioral sensitization to dopamine D(2) receptor agonists.

To assess the possible modulatory effects of noradrenergic and serotoninergic neurons on dopaminergic neuronal activity, the noradrenergic and serotoninergic neurotoxins DSP-4 N-(2-chlorethyl)-N-ethyl-2-bromobenzylamine (50.0 mg/kg, sc) and 5,7-dihydroxytryptamine (5,7-DHT) (37.5 microg icv, half in each lateral ventricle), respectively, were administered toWistar rats on the first and third days of postnatal ontogeny, and dopamine (DA) agonist-induced behaviors were assessed in adulthood. At eight weeks, using an HPLC/ED technique, DSP-4 treatment was associated with a reduction in NE content of the corpus striatum (> 60%), hippocampus (95%), and frontal cortex (> 85%), while 5,7-DHT was associated with an 80-90% serotonin reduction in the same brain regions. DA content was unaltered in the striatum and the cortex. In the group lesioned with both DSP-4 and 5,7-DHT, quinpirole-induced (DA D(2) agonist) yawning, 7-hydroxy-DPAT-induced (DA D(3) agonist) yawning, and apomorphine-induced (non-selective DA agonist) stereotypies were enhanced. However, SKF 38393-induced (DA D(1) agonist) oral activity was reduced in the DSP-4 + 5,7-DHT group. These findings demonstrate that DA D(2)- and D(3)-agonist-induced behaviors are enhanced while DA D(1)-agonist-induced behaviors are suppressed in adult rats in which brain noradrenergic and serotoninergic innervation of the brain has largely been destroyed. This study indicates that noradrenergic and serotoninergic neurons have a great impact on the development of DA receptor reactivity (sensitivity).

Blood pressure references for Polish children and adolescents.

The objective of this study was to develop age- and gender-specific reference ranges for blood pressure in a large national database on blood pressure levels throughout childhood and adolescence in young Poles. A prospective cross-sectional study was performed in 2002-2005 in the representative sampling sites, selected randomly from the entire Poland. Altogether, 6,447 school pupils, aged 7-18 years, were involved in the study of which 3,176 were boys and 3,271 were girls. Statistical analysis was performed using STATISTICA for Windows 7.1. The normal range of blood pressure, determined by age and the category of body height percentiles, revealed percentiles values which might serve as reference values to identify cases of high normal blood pressure (the mean blood pressure between 90th and 95th percentiles for age and gender) and hypertension (the mean blood pressure equals or exceeds the 95th percentiles on at least three occasions).

Neonatal N-(-2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) treatment modifies the vulnerability to phenobarbital- and ethanol-evoked sedative-hypnotic effects in adult rats.

To study the influence of the central noradrenergic system on sensitivity to sedative-hypnotic effects mediated by the aminobutyric acid (GABA) system, intact rats were contrasted with rats in which noradrenergic nerves were largely destroyed shortly after birth with the neurotoxin DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine; 50 mg/kg sc x2, P1 and P3]. At 10 weeks, loss of the righting reflex (LORR) was used as an index to study the acute sedative-hypnotic effects of phenobarbital (100 mg/kg ip) and ethanol (4 g/kg ip, 25% v/v). Additionally, GABA concentration in the medial prefrontal cortex (PFC), hippocampus, cerebellum and brainstem was estimated by an HPLC/ED method. Neonatal DSP-4 treatment diminished the sedative-hypnotic effects of both phenobarbital and ethanol in adult rats. While the endogenous GABA content in the PFC, hippocampus, brainstem and cerebellum of DSP-4-treated rats was not altered, phenobarbital significantly decreased GABA content of both intact and DSP-4-lesioned rats by approximately 40% in the hippocampus and by approximately 20% in other brain regions at 1 h. Ethanol reduced GABA content by approximately 15-30% but only in the hippocampus and brainstem of both intact and lesioned rats. These findings indicate that the noradrenergic system exerts a prominent influence on sedative-hypnotics acting via GABAergic systems in the brain without directly altering GABA levels in the brain.

Ontogenetic noradrenergic lesion alters histaminergic activity in adult rats.

To determine whether noradrenergic nerves might have a modulatory role on the sensitivity or reactivity of histaminergic receptor systems in brain, behavioral effects of the respective histamine H1, H2 and H3 antagonists S(+)chlorpheniramine, cimetidine and thioperimide in control adult rats were compared to the effects in adult rats that had been lesioned as neonates with the noradrenergic neurotoxin DSP-4. On the 1st and 3rd days after birth rat pups were treated with either saline or DSP-4 (50 mg/kg sc), then returned to their home cages with the dam. At 8 weeks when rats were tested, S(+)chlorpheniramine (10 mg/kg ip) was found to increase locomotor activity in intact and DSP-4 lesioned rats, while cimetidine (5 mg/kg, ip) and thioperimide (5 mg/kg, ip) increased activity several-fold solely in the DSP-4 group. Exploratory activity, nociceptive activity, and irritability were little altered by the histamine antagonists, although oral activity was increased by thioperimide in intact and lesioned rats, and by cimetidine or S(+)chlorpheniramine in DSP-4 rats. High performance liquid chromatography with electrochemical detection was used to determine that DSP-4 produced a 90% reduction in frontal cortex, hippocampus and hypothalamus, with a 90% elevation of NE in cerebellum--reflecting reactive sprouting of noradrenergic fibers consequent to lesion of noradrenergic tracts projecting to proximal brain regions. These findings indicate that perinatal noradrenergic fiber lesioning in rat brain is associated with an altered behavioral spectrum by histamine H1, H2 and H3 receptor antagonists, thereby implicating histaminergic systems as modulators of noradrenergic systems in brain.

Cortical dopaminergic neurotransmission in rats intoxicated with lead during pregnancy. Nitric oxide and hydroxyl radicals formation involvement.

It is well established that low level Pb-exposure is associated with a wide range of cognitive and neurobehavioral dysfunctions in children. In fact, Pb-induced damage occurs preferentially in the prefrontal cerebral cortex, hippocampus and cerebellum - the anatomical sites which are crucial in modulating emotional response, memory and learning. Previously it was also shown that nitric oxide (NO) signaling pathway as well as glutamatergic neurotransmission are both involved in brain development, neurotoxicity and neurodegeneration processes whereas Pb(2+) interfere with both. For this reason we investigated the effect of ontogenetic Pb(2+) exposure on dopaminergic neurotransmission in the medial prefrontal cortex (mPFC) of rats after amphetamine (AMPH) and/or 7-nitroindazole (7-NI) administration. Furthermore, the possible role of oxidative stress in Pb(2+)-induced neurotoxicity in prenatally Pb(2+)-treated rats was explored in the content of hydroxyl radical (HO) species in mPFC after AMPH and/or 7-NI injection, assessed by HPLC analysis of 2.3-dihydroxybenzoic acid (2.3-DHBA) - spin trap product of salicylate. As shown, the results of this study suggest that Pb(2+) exposure during intrauterine life did not substantially affect cortical dopaminergic neurotransmission in adult offspring rats evaluated by means of microdialysis of mPFC and the content of the cortical HO. It is likely that striatum, nucleus accumbens or other dopamine rich brain areas are more intricately associated with Pb(2+) precipitated behavioral, dopamine - dependent impairments observed in mammalians.

[Pioneers of anaesthesiology--Arthur Ernest Guedel (1883-1956)]. / Pionierzy anestezjologii--Arthur Ernest Guedel (1883-1956).

Arthur Ernest Guedel was a US born anaesthetist, whose name found its place among key persons in our specialty. Commonly known as a developer of the oropharyngeal airway, he did much more. Possibly, his major achievements were the detailed description of nitrous oxide and diethyl ether anaesthesia. He was among the firstfull-time US anaesthesiologists, and also served in his profession during the First World War. So called Guedel charts, describing the relationship between the level of anaesthesia and pupillary reactions, allowed many non-anaesthesiologists to administer diethyl ether relatively safely. Together with Waters, he was among pioneers of cuffed endotracheal tubes. At the end of his career, in 1937, he produced a manual "Inhalational Anaesthesia--A Fundamental Guide, which served at least three generations of medical professionals.

[Corticosteroids effect on angiogenesis in heart muscle]. / Wplyw kortykosteroidów na angiogeneze w miesniu sercowym.

The process of angiogenesis in a heart muscle is a way of providing the ischaemic myocardium with oxygen and nutritive ingredients. This natural process called therapeutic angiogenesis has been tried in the treatment of patients with coronary artery disease mainly. It has been seen as a chance of an effective beneficial therapy particularly in these patients for whom pharmacological treatment is not sufficient and who are disqualified for operative methods such as the percutaneous coronary angioplasty, or coronary bypass transplantation. The goal of therapeutic angiogenesis is to stimulate the growth of new capillaries in a heart and, as a result, to improve the perfusion and function of a heart muscle. The positive impact of the angiogenesis in a heart muscle is impeded in patients using corticosteroids in treatment for other illnesses. Corticosteroids inhibit the angiogenesis process on a cellular and tissue level. They decrease gene expression for VEGF, iNOS, inhibit the activity of transcriptive factors for AP-1 and NF(k)B. Corticosteroids cause the degradation of a pericellular matrix, inhibit the migration of macrophages and inhibit the synthesis of NO and interleukin. These activities of corticosteroids decrease the number of new vessels in a ischaemic myocardium and, consequently, worsen vascularization and progressive hypoxia.

Nitric oxide modulates the amphetamine effect on [3H]glucose uptake in the brain of rats prenatally exposed to lead.

Glucose is the main source of energy for the central nervous system (CNS). In this study, we examined the effects of the psychostimulant amphetamine (AMPH) and the neuronal mediator nitric oxide (NO) on [3H]glucose uptake in the brain of adult rats that had been prenatally exposed to lead. Lead [Pb(CH3COO)2 . 3H2O; 250 ppm] was added to the drinking water of pregnant Wistar rats for the duration of pregnancy. On the day of parturition, lead was discontinued as an additive in the drinking water. Offspring remained ith dams for 21 days. The control group consisted of rats that consumed water without lead. In adulthood, male offspring from both groups (lead-exposed and control) were pretreated with 7-nitroindazole (nNOS blocking agent) (10.0 mg/kg ip) or saline (1.0 ml/kg ip), 30 min before AMPH (1.0 mg/kg ip). After another 30 min, and 15 min before termination, all rats were injected with 6-[3H]-D-glucose (500 muCi/kg ip). Brain specimens were taken (striatum, frontal cortex, hippocampus, and thalamus with hypothalamus, and pons with medulla oblongata) for determination of radioactivity in a liquid scintillation counter. We found that lead did not alter [3H]glucose uptake in brain regions studied (with exception of frontal cortex) but that AMPH increased [3H]glucose uptake in the striatum, frontal cortex and hippocampus, and that the AMPH effect was lessened in the hippocampus of lead-exposed rats. Moreover, the AMPH effect on [3H]glucose uptake in the frontal cortex, hippocampus, thalamus with hypothalamus and pons of control rats was potentiated by 7-NI pretreatment. Similar effect was observed in lead-intoxicated rats (striatum, frontal cortex and hippocampus). These results indicate that NO modulates AMPH-induced [3H]glucose uptake in the brain of rats prenatally exposed to lead.

[Smoking and drug use among students of selected univerities]. / Palenie tytoniu i stosowanie innych uzywek wsr6ód studentów wybranych uczelni.

Smoking, drinking alcohol and drugs are still actual social and health problems in Poland and in the world as well. Conducted studies, considering health behaviours among children and youth, indicate high percentage (between 20-30%) of smokers in mentioned population, depending on age, gender and environment. Health effects caused by smoking occur usually in adulthood as smoking related diseases, despite the addiction leading to the health problem begins earlier, even in childhood. Statistics, considering drinking alcohol and drugs abuse among young people are also frightening. The aim of the study was to evaluate and compare the state of knowledge about harmful effects of smoking, drinking alcohol and drugs use among students of Silesian Medical University, Silesian University of Technology and Academy of Physical Education and to evaluate and compare health attitudes towards mentioned addictions among students of different Universities. 315 students at age between 19-24 years took part in the study and filled in the anonymous questionnaire prepared by authors. Surveyed population included 108 students of Silesian Medical University, 110 students of Silesian University of Technology and 97 students of Academy of Physical Education in Katowice. Knowledge, presented by all students, about harmful effects of smoking, drinking alcohol and drugs use is not put into practice and does not result in healthy behaviours in examined part of life style. Students of Silesian Medical University demonstrate the highest state of knowledge about drugs. Students of Academy of Physical Education in Katowice have the most improper behaviours in the area of addictions. There is a necessity of preparing and spreading efficacious prophylactic programmes in order to raise awareness about the harmfulness of smoking, drinking and drugs use.

The neuroprotective function of vascular endothelial growth factor (VEGF).

The vascular endothelial growth factor (VEGF) is known mainly as the potent angiogenic and vascular permeability-enhancing factor. Both processes are very effective in hypoxia. The latest studies show that VEGF has neurotrophic and neuroprotective as well as angiogenic properties. It exerts neuroprotective actions directly through the inhibition of programmed cell death (PCD), or apoptosis and the stimulation of neurogenesis. VEGF is also a mediator of multiple processes including angiogenesis, enhancing blood brain barrier permeability for glucose, antioxidants activation, which indirectly result in neuroprotection. VEGF prevents neurons from death under critical conditions such as hypoxia, glucose deprivation through binding to the specific receptors, which are also expressed on the surface of neuronal cells. The increased expression of VEGFR-2/flk-1/KDR receptors on neurons subjected to hypoxia, glucose deprivation provides evidence that these receptors are mainly involved in neuroprotective effects of VEGF. Furthermore, binding to these receptors triggers the phosphatidyloinositol 3-kinase (PI3K) /Akt signal transduction system and, in consequence, leads to the inhibition of PCD by activating antiapoptotic proteins through the transcription factor NFkappaB and inhibiting proapoptotic signaling by Bad, caspase-9, caspase-3, and other effectors. Promotion of neuronal cells proliferation by VEGF is also associated with the increased expression of VEGFR-2 receptors and up-regulation of E2F family transcription factors, cyclin D1, cyclin E, and cdc25. It is known that the amount and types of VEGF isoforms influence its action. At least six isoforms of VEGF proteins are formed as a result of alternative mRNA splicing and it is unknown which of them and in what proportion occur in the nervous system in physiology and pathophysiology. It seems to be very essential to find out the mechanisms responsible for specific patterns of VEGF isoforms and their receptors expression in different pathologies of the nervous system. Maybe such knowledge will provide new perspectives in VEGF therapy.

[Evaluation of knowledge and health attitude towards cigarette smoking, alcohol and drugs use among students]. / Ocena wiedzy i postaw zdrowotnych studentów w zakresie palenia tytoniu i stosowania innych uzywek.

Cigarette smoking, drinking alcohol and drug use are important epidemiological problems affecting state of health. Negative effects of these unhealthy behaviors are commonly known and result in many socioeconomic consequences. Despite relatively good knowledge about harm-fullness of cigarette smoking a percentage of smokers in polish population is still high, especially in young population, and hesitates between 20-30% depending on age, sex and socioeconomic conditions. Negative health attitude towards smoking, drinking alcohol and drug use among young people requires further education and promotion in this area. Aim of the study was evaluation of knowledge about harmful effects of smoking, drinking alcohol and drug use among students of Silesian University of Technology and evaluation of health attitudes towards smoking, drinking alcohol and drug abuse in examined population. 109 students of Silesian University of Technology at age between 19-24 years took part in the study and filled the anonymous questionnaire prepared by authors. The study revealed that 8% of Silesian University of Technology students smoke cigarettes regularly. 15% of students declare smoking occasionally despite most of them know negative effects of such smoking. Almost 80% do not smoke at all. In opinion of 66,7% passive model of smoking is as harmful as the active one. Relatively many (8%) of examined students admit drinking alcohol regularly. Only 15% do not drink alcohol. 35% of students declare taking a drug, at least once during entire life, and some of examined consider marihuana as not addictive. High knowledge about harmful effects of smoking among students results in a relatively low percentage of inveterate smokers. Despite knowledge about harmfulness of drinking alcohol and drug abuse proper healthy behaviors in this area are not put into practice in examined motion in order to reduce unhealthy behaviors among young people.

Increase of the IL-1 beta and IL-6 levels in CSF in patients with vasospasm following aneurysmal SAH.

Cytokines play a key role in mutual influence of the immunological, endocrine and CNS systems. It has been proven that proinflammatory ILs may intensify the cascade of biochemical changes in ischemic brain damage. Vasospasm, which may accompany SAH and often coexists with symptoms of DINDs, is the cause of ischemic changes in the brain. It is thought that immunological mechanisms may be one of the causes of degenerative-productive changes in vessel walls, in delayed vasospasm following SAH, which lead to substantial vasospasm and in consequence too cerebral ischemia. In the randomly selected group of patients, who underwent surgical treatment after aneurysmal SAH, we determined the concentration of IL-1 beta and IL-6 in CSF in the periods between Days 0 to 3; 4 to 7; and 8 to 15 after the occurrence of SAH. The presence and dynamics of development of vasospasm were assessed on the basis of increasing DINDs as well as CT and cerebral angiography. We examined the concentrations of ILs in CSF using radioimmunological methods, applying commercially available tests for their assessment. We found that in the period between 8 and 15 days after SAH, in increasing delayed vasospasm and DINDs, here is a statistically significant increase concentration of IL-1 beta in CSF (105.4 +/- 46.9 pg x ml-1; p<0.005), and no significant changes in patients without vasospasm and neurological deficits. On the other hand, we noted a statistically significant increase concentration of IL-6 in CSF (4802 +/- 1170 ng x ml-1; p<0.05) only in the acute phase after SAH (Days 0-3) in patients in poor clinical condition, in whom delayed vasospasm and cerebral ischemia developed later. This increase of ILs level in CSF is probably related to the intensity of the SAH, and secondarily aggravates the vasospasm and ischemic changes in the brain.

Transcription factors having impact on vascular endothelial growth factor (VEGF) gene expression in angiogenesis.

This article discusses the role of transcription factors in vascular endothelial growth factor (VEGF) gene expression. Angiogenesis is a complex and multilevel process of new capillary formation on the basis of already existing blood vessels. Physiologically, it is a very strictly regulated process, which results in a balance between stimulatory (angiogenic) and inhibitory (angiostatic) factors to control the correct development of blood vessels. There are many very well characterized angiogenic and angiostatic factors that can modulate VEGF expression. Some of them (e.g. HIF-1, AP-1, and Sp-1) are transcription factors, proteins that bind to the VEGF promoter to initiate and activate the transcription of a gene directly. Others, like nitric oxide or cytokines, are agents that stimulate the transcription factors through different cellular signaling pathways. There are also oncogenes (V-SRC, bcl-2) and tumor suppressor genes (VHL), the mutations of which lead indirectly to increased transcription of the VEGF gene.

The role of vascular endothelial growth factor in cerebral oedema formation.

Cerebral oedema induced by hypoxia is connected with activity of vascular endothelial growth factor (VEGF). Hypoxia activates VEGF expression, which leads to the increase of endothelial permeability. Hypoxia-induced VEGF overexpression is connected with transcriptional activation by hypoxia-inducible factor 1 (HIF-1) and posttranscriptional stabilisation of mRNA by proteins such as HuR. Also a number of VEGF receptors increases in response to hypoxia. Transcriptional activation by HIF-1 (receptor flt-1) and posttranscriptional mechanism (receptor KDR) play a key role in this process. Vascular endothelial growth factor increases the permeability and this process is very effective in hypoxia, which prevents the rapid autooxidation of the second messenger NO. Many VEGF inhibitors can be used in future for prevention or treatment of hypoxia-induced cerebral oedema. They can inhibit VEGF formation (as used in cerebral oedema dexamethason, or barbiturates, trichstatin A, candesartan, small molecule inhibitors of hypoxia-inducible factor 1, gelandamycin, antysenses, rybosymes and catechins) or VEGF activity (soluble receptors, monoclonal antibodies, heterodimeric antagonistic VEGF variant, RTK inhibitors and catechins).