Octopamine is involved in TRP-induced thermopreference responses in American cockroach.

Insects' thermoregulatory processes depend on thermosensation and further processing of thermal information in the nervous system. It is commonly known that thermosensation involves thermoreceptors, including members of the TRP receptor family, but the involvement of neurotransmitters in thermoregulatory pathways remains unstudied. We conducted test to determine whether octopamine, a biogenic amine that acts as a neurotransmitter and neurohormone in insects, is involved in TRP-induced thermoregulatory responses in Periplaneta americana. We used capsaicin, an activator of the heat-sensitive TRP channel, Painless, to induce thermoregulatory response in cockroaches. Then, we evaluated the behavioural (thermal preferences and grooming), physiological (heart rate) and biochemical responses of insects to capsaicin, octopamine and phentolamine - octopaminergic receptor blocker. Capsaicin, similar to octopamine, increased cockroaches' grooming activity and heart rate. Moreover, octopamine level and protein kinase A (PKA) activity significantly increased after capsaicin treatment. Blocking octopaminergic receptors with phentolamine diminished cockroaches' response to capsaicin - thermoregulatory behaviour, grooming and heart rate were abolished. The results indicate that octopamine is a neurotransmitter secreted in insects after the activation of heat receptors.

Sublethal biochemical, behavioral, and physiological toxicity of extremely low dose of bendiocarb insecticide in Periplaneta americana (Blattodea: Blattidae).

Insecticides are dedicated to impair the insect organisms, but also have an impact on other, non-target organisms, including humans. In this way, they became important risk factor for disturbance of physiological homeostasis and can be involved in the development of diseases or in deterioration of existing conditions. The influence of sublethal doses of various insecticides on vertebrates' and invertebrates' organisms has been previously observed. In this paper, we have evaluated the impact of exposure to extremely low dose of neurotoxin, bendiocarb (0.1 nM), a commonly used carbamate insecticide on a model organism in neurobiology-Periplaneta americana. The assessment was performed on all levels of animal organism from molecular (oxidative stress parameters: phosphorylation level of proteins, cAMP level, protein kinase A and C levels, and octopamine) to physiological (heart beat and gas exchange tests) and behavioral (motor skills assay, grooming test). Exposure to such a low level of bendiocarb did not cause direct paralysis of insects, but changed their grooming behavior, decreased heart rate, and increased gas exchange. We also observed the increased parameters of oxidative stress as well as stressogenic response to 0.1 nM bendiocarb exposure. Exposure to a trace amount of bendiocarb also increased sensitivity to effective doses of the same insecticide, thus acts as preconditioning. These results force us to reconsider the possible risk from frequent/continuous exposure to traces of pesticide residues in the environment to human health.

New View on the Impact of the Low-Frequency Electromagnetic Field (50 Hz) on Stress Responses: Hormesis Effect.

INTRODUCTION: Low-frequency electromagnetic field (50 Hz) (EMF) can modify crucial neuronal processes. Existing data indicate that exposure to EMF may represent a mild stressor and contribute to disturbances of the hypothalamic-pituitary-adrenal (HPA) axis. The important regulatory pathways controlling HPA axis activity include two types of corticosteroid receptors: mineralocorticoid receptors (MRs) and glucocorticoid receptors. They are particularly abundant in the hippocampus, a key locus of HPA axis feedback control. The research aimed at determining whether (1) EMF exhibits hormesis, it means bidirectional action depending on EMF intensity (1 or 7 mT) and (2) repeated EMF exposure changes stress response to subsequent stress factors. METHODS: The exposure (7 days, 1 h/day) of adult rats to EMF (1 mT and 7 mT) was repeated 3 times. HPA axis hormones and their receptors were analysed after each following exposure. Moreover, the impact of EMF exposure on hormonal and behavioural responses to subsequent stress factor - open-field test was evaluated. RESULTS: Our data suggest that exposure to EMF can establish a new "set-point" for HPA axis activity. The direction and dynamics of this process depend on the intensity of EMF and the number of exposures. EMF of 1 mT induced an adaptive stress response, but 7 mT EMF caused sensitization. Consequently, EMF changed the vulnerability of the organism to a subsequent stress factor. We have also shown the increase in MR mRNA abundance in the hippocampus of 1 mT EMF-exposed rats, which can represent the possible neuroprotective response and suggest therapeutic properties of EMFs.

Bidirectional Effect of Repeated Exposure to Extremely Low-Frequency Electromagnetic Field (50 Hz) of 1 and 7 mT on Oxidative/Antioxidative Status in Rat's Brain: The Prediction for the Vulnerability to Diseases.

Studies reported evidence for opposite effects of extremely low-frequency electromagnetic field (EMF): harmful, including the oxidative stress induction, and beneficial, such as the activation of antioxidant defense. People's exposure to EMF is often repeated or prolonged, and it is important to consider the cumulative effect of such kind of exposure on the organism. If changes evoked by repeated exposure to EMF are permanent, responsiveness to other stress factors can be modified. The aims of our study were (1) to evaluate changes in the levels of oxidative stress and antioxidant defense markers in the prefrontal cortex of adult rats after repeated exposure to 1 and 7 mT EMF and (2) to assess whether repeated EMF exposure can modify oxidative/antioxidative status in response to other stress factors. Rats were exposed to EMF 1 h/day for 7 days, one, twice, or three times. After each exposure, 8-isoprostanes, protein carbonyl groups, and the total antioxidant capacity were assessed. Part of the animals, after EMF treatment, was exposed to another stress factor-open field. Results showed that repeated exposure changed the oxidative/antioxidative status depending on the intensity of the EMF and the number of exposures. 1 mT EMF created weak changes in the oxidative status in the brain; however, 7 mT EMF moved the balance to a clearly higher level. The changes in the oxidative status after 1 mT EMF were enough to reduce, and after 7 mT EMF to intensify oxidative processes in response to the next stress. We concluded that the organism might adapt to "weak" EMF, while "strong" EMF exceeds the adaptive capacity of the organism and sensitizes it to subsequent stress, and thus may modulate vulnerability to diseases. Our results also provide new insights into the possible therapeutic properties of the magnetic field, as 1 mT EMF appears to have a potentially protective impact on the brain.

Electromagnetic field and TGF-ß enhance the compensatory plasticity after sensory nerve injury in cockroach Periplaneta americana.

Recovery of function after sensory nerves injury involves compensatory plasticity, which can be observed in invertebrates. The aim of the study was the evaluation of compensatory plasticity in the cockroach (Periplaneta americana) nervous system after the sensory nerve injury and assessment of the effect of electromagnetic field exposure (EMF, 50 Hz, 7 mT) and TGF-ß on this process. The bioelectrical activities of nerves (pre-and post-synaptic parts of the sensory path) were recorded under wind stimulation of the cerci before and after right cercus ablation and in insects exposed to EMF and treated with TGF-ß. Ablation of the right cercus caused an increase of activity of the left presynaptic part of the sensory path. Exposure to EMF and TGF-ß induced an increase of activity in both parts of the sensory path. This suggests strengthening effects of EMF and TGF-ß on the insect ability to recognize stimuli after one cercus ablation. Data from locomotor tests proved electrophysiological results. The takeover of the function of one cercus by the second one proves the existence of compensatory plasticity in the cockroach escape system, which makes it a good model for studying compensatory plasticity. We recommend further research on EMF as a useful factor in neurorehabilitation.

Extremely Low-Frequency Magnetic Field as a Stress Factor-Really Detrimental?-Insight into Literature from the Last Decade.

Biological effects of extremely low-frequency magnetic field (ELF-MF) and its consequences on human health have become the subject of important and recurrent public debate. ELF-MF evokes cell/organism responses that are characteristic to a general stress reaction, thus it can be regarded as a stress factor. Exposure to ELF-MF "turns on" different intracellular mechanisms into both directions: compensatory or deleterious ones. ELF-MF can provoke morphological and physiological changes in stress-related systems, mainly nervous, hormonal, and immunological ones. This review summarizes the ELF-MF-mediated changes at various levels of the organism organization. Special attention is placed on the review of literature from the last decade. Most studies on ELF-MF effects concentrate on its negative influence, e.g., impairment of behavior towards depressive and anxiety disorders; however, in the last decade there was an increase in the number of research studies showing stimulating impact of ELF-MF on neuroplasticity and neurorehabilitation. In the face of numerous studies on the ELF-MF action, it is necessary to systematize the knowledge for a better understanding of the phenomenon, in order to reduce the risk associated with the exposure to this factor and to recognize the possibility of using it as a therapeutic agent.

How to Improve the Antioxidant Defense in Asphyxiated Newborns-Lessons from Animal Models.

Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial. Pharmacotherapy with deferoxamine (DFO) is commonly recognized as a beneficial regimen for H/I insult. DFO, via iron chelation, reduces oxidative stress. It also assures an optimal antioxidant protection minimizing depletion of the antioxidant enzymes as well as low molecular antioxidants. In the present review, some aspects of recently acquired insight into the therapeutic effects of hypothermia and DFO in promoting neuronal survival after H/I are discussed.

Decreased body temperature during anoxia affects the endogenous BDNF level in tertiary phase of injury.

Asphyxia before, during, or after birth is an important cause of perinatal mortality and morbidity. The mechanism underlying neurological damage resulting from anoxia episode is complex and is not limited to the anoxia episode. Although the benefits of therapeutic hypothermia in secondary failure of oxidative metabolism have long been known, the principle of this therapy in tertiary phase of repair and reorganization have not yet to be fully elucidated. Currently brain-derived neurotrophic factor (BDNF) is also considered to be beneficial to neuronal survival. Therefore, our experiments aimed at determining the effects of low body temperature during simulated perinatal anoxia on the level of the neurotrophic brain-derived factor (BDNF) and on the correlation between the level of BDNF (proBDNF and mBDNF) and the level of active caspase-3 (marker of apoptosis) in developing brain in tertiary phase after exposure. The results demonstrated that the ability of BDNF to inhibit caspase-3 activation and subsequent apoptosis likely accounts in large part for its protection against neuronal damage only in rats maintaining the low body temperature.

Thermal conditions during neonatal anoxia affect the endogenous level of brain-derived neurotrophic factor.

Anoxia during delivery is a complication that can disturb infant brain development leading to various types of neurological disorders. Our studies have shown that increased body temperature of newborn rats of both sexes intensifies the postanoxic oxidative stress and prevents triggering the endogenous adaptive response such as HIF-1α activation. Currently, brain-derived neurotrophic factor-BDNF is considered to be a modulator of neuronal plasticity. In the developing brain, mature BDNF and its precursor exhibit prosurvival action through the TrkB receptor and proapoptotic functions binding to p75NTR , respectively. The aim of our experiments was to check the effects of body temperature on the postanoxic level of BDNF and on the expression of its receptors as well as on the marker of apoptosis-caspase-3 in the rat brain. Two-day-old Wistar Han rats (male/female ratio, 1:1) were exposed to anoxia in 100% nitrogen atmosphere for 10 min in different thermal conditions, which allowed them to regulate their rectal temperature at the following levels: normothermic-33°C; hyperthermic-37°C; and extremely hyperthermic-39°C. Thermal conditions during neonatal anoxia affected the level of proBDNF, BDNF as well as their receptors and caspase-3 in the forebrain. The increased BDNF protein level followed by decreased caspase-3 protein level was probably dependent on body temperature under anoxic conditions and was observed only in rats maintaining decreased body temperature. The positive effect of BDNF was not observed under hyperthermic conditions. Moreover, BDNF level changes correlated with body temperature probably affected the learning and spatial memory in juvenile rats.

Capsaicin-induced dysregulation of acid-base status in the American cockroach.

Members of TRP receptor family are involved in response to acidification. Here, we determined the effect of capsaicin, one of the TRP receptor activators, on hemolymph acid-base status in the American cockroach. Periplaneta americana adult individuals were injected with lactic acid (5% or 10%) and exposed to 100 µM capsaicin solution. Hemolymph pH was measured 15 min, 1, 4, 8 and 24 h after lactic acid and capsaicin application with a glass microelectrode. The results demonstrated that cockroaches recover from acidosis within 4 h from acid injection. Capsaicin impaired the buffering capacity of insects' hemolymph, resulting in significant drop of hemolymph pH observed even 24 h after application. Joint action of capsaicin and acidosis reveals new insight into possible mechanism of capsaicin action on TRP receptors in insects.

Effect of Capsaicin and Other Thermo-TRP Agonists on Thermoregulatory Processes in the American Cockroach.

Capsaicin is known to activate heat receptor TRPV1 and induce changes in thermoregulatory processes of mammals. However, the mechanism by which capsaicin induces thermoregulatory responses in invertebrates is unknown. Insect thermoreceptors belong to the TRP receptors family, and are known to be activated not only by temperature, but also by other stimuli. In the following study, we evaluated the effects of different ligands that have been shown to activate (allyl isothiocyanate) or inhibit (camphor) heat receptors, as well as, activate (camphor) or inhibit (menthol and thymol) cold receptors in insects. Moreover, we decided to determine the effect of agonist (capsaicin) and antagonist (capsazepine) of mammalian heat receptor on the American cockroach's thermoregulatory processes. We observed that capsaicin induced the decrease of the head temperature of immobilized cockroaches. Moreover, the examined ligands induced preference for colder environments, when insects were allowed to choose the ambient temperature. Camphor exposure resulted in a preference for warm environments, but the changes in body temperature were not observed. The results suggest that capsaicin acts on the heat receptor in cockroaches and that TRP receptors are involved in cockroaches' thermosensation.

Electromagnetic field exposure (50 Hz) impairs response to noxious heat in American cockroach.

Exposure to electromagnetic field (EMF) induces physiological changes in organism that are observed at different levels-from biochemical processes to behavior. In this study, we evaluated the effect of EMF exposure (50 Hz, 7 mT) on cockroach's response to noxious heat, measured as the latency to escape from high ambient temperature. We also measured the levels of lipid peroxidation and glutathione content as markers of oxidative balance in cockroaches exposed to EMF. Our results showed that exposure to EMF for 24, 72 h and 7 days significantly increases the latency to escape from noxious heat. Malondialdehyde (MDA) levels increased significantly after 24-h EMF exposure and remained elevated up to 7 days of exposure. Glutathione levels significantly declined in cockroaches exposed to EMF for 7 days. These results demonstrate that EMF exposure is a considerable stress factor that affects oxidative state and heat perception in American cockroach.

Altered heat nociception in cockroach Periplaneta americana L. exposed to capsaicin.

Some natural alkaloids, e.g. capsaicin and camphor, are known to induce a desensitization state, causing insensitivity to pain or noxious temperatures in mammals by acting on TRP receptors. Our research, for the first time, demonstrated that a phenomenon of pharmacological blockade of heat sensitivity may operate in American cockroach, Periplaneta americana (L.). We studied the escape reaction time from 50°C for American cockroaches exposed to multiple doses of different drugs affecting thermo-TRP. Capsaicin, capsazepine, and camphor induced significant changes in time spent at noxious ambient temperatures. Moreover, we showed that behavioral thermoregulation in normal temperature ranges (10-40°C) is altered in treated cockroaches, which displayed a preference for warmer regions compared to non-treated insects. We also measured the levels of malondialdehyde (MDA) and catalase activity to exclude the secondary effects of the drugs on these processes. Our results demonstrated that increase in time spent at 50°C (five versus one trial at a heat plate) induced oxidative stress, but only in control and vehicle-treated groups. In capsaicin, capsazepine, menthol, camphor and AITC-treated cockroaches the number of exposures to heat had no effect on the levels of MDA. Additionally, none of the tested compounds affected catalase activity. Our results demonstrate suppression of the heat sensitivity by repeated capsazepine, camphor and capsaicin administration in the American cockroach.

Activation of hypoxia-inducible factor-1α in rat brain after perinatal anoxia: role of body temperature.

Transcriptional hypoxia-inducible factor-1α (HIF-1α) plays the fundamental role in adaptive processes in response to hypoxia. Specific HIF-1α target genes are involved in glycolysis, erythropoiesis and angiogenesis to promote survival. In our previous study we have demonstrated that naturally low body temperature of newborn rats protects them against damage due to perinatal hypoxia. Therefore, our experiments aimed at checking the effects of body temperature during simulated perinatal anoxia on subsequent changes of expression of HIF-1α and its specific target genes such as vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in the rat brain. Two-day old Wistar rats were divided into three temperature groups: normothermic -33 °C, hyperthermic -37 °C and extremely hyperthermic -39 °C. The temperature was controlled 15 min before start and continued during 10 min of anoxia as well as for 2 h post-anoxia. HIF-1α was analysed by Western blot and immunofluorescence and mRNA levels of HIF-1α and its downstream genes (VEGF, EPO) were quantified by qRT-PCR. Thermal conditions during neonatal anoxia affected the hippocampal and neocortical level of HIF-1α protein. Physiological body temperature of newborn rats led to prominent accumulation of cerebral HIF-1α protein and significant upregulation of VEGF and EPO mRNA. In contrast, anoxia-induced HIF-1α activation at elevated body temperatures was less pronounced. Since HIF-1α and EPO have recently been regarded as promising therapeutical targets against brain lesions due to hypoxia/ischemia, presented data imply that in order to achieve a full effect of neuroprotection, the thermal conditions during and after the insult should be taken into consideration.

Molecular Targets for Components of Essential Oils in the Insect Nervous System-A Review.

Essential oils (EOs) are lipophilic secondary metabolites obtained from plants; terpenoids represent the main components of them. A lot of studies showed neurotoxic actions of EOs. In insects, they cause paralysis followed by death. This feature let us consider components of EOs as potential bioinsecticides. The inhibition of acetylcholinesterase (AChE) is the one of the most investigated mechanisms of action in EOs. However, EOs are rather weak inhibitors of AChE. Another proposed mechanism of EO action is a positive allosteric modulation of GABA receptors (GABArs). There are several papers that prove the potentiation of GABA effect on mammalian receptors induced by EOs. In contrast, there is lack of any data concerning the binding of EO components in insects GABArs. In insects, EOs act also via the octopaminergic system. Available data show that EOs can increase the level of both cAMP and calcium in nervous cells. Moreover, some EO components compete with octopamine in binding to its receptor. Electrophysiological experiments performed on Periplaneta americana have shown similarity in the action of EO components and octopamine. This suggests that EOs can modify neuron activity by octopamine receptors. A multitude of potential targets in the insect nervous system makes EO components interesting candidates for bio-insecticides.

Rubella in Poland in 2014

BACKGROUND: In 2004, Poland has adopted the WHO goal of rubella elimination and congenital rubella syndrome prevention. The main target of the Programme is to stop transmission of the virus in the environment and prevention of congenital rubella in children. In Poland participation in the rubella elimination program requires clinical diagnosis of rubella cases and their confirmation with laboratory tests. Vaccination against rubella was introduced in 1987, initially only in 13 - year-old girls. Since 2003, single jab vaccination against rubella, measles and mumps is used (MMR vaccine for all children: primary vaccination at the age 13-15 months and a booster vaccination at the age of 10). AIM: To assess epidemiological situation of rubella in Poland in 2014, including vaccination coverage in Polish population. MATHERIAL AND METHODS: The descriptive analysis was based on data retrieved from routine mandatory surveillance system and published in the annual bulletins "Infectious diseases and poisonings in Poland in 2014" and "Vaccinations in Poland in 2014" (MP. Czarkowski, Warszawa 2014, NIZP-PZH, GIS). RESULTS: In 2014, there was a significant decrease in the number of rubella cases - with registered 5891 cases (in 2013 - 38 548 cases) - and a decline in incidence (from 101.1 per 100 000 to 15.3). The highest incidence, regardless of gender and the environment was observed in the age group 5-6 years (respectively 93.8 and 109.4 per 100 000). Similarly to 2013, rubella incidence of males was higher than the incidence in girls and women (20.0 versus 10.9). In 2014, no cases of congenital rubella syndrome were registered. SUMMARY AND CONCLUSIONS: The proportion of laboratory tests confirming/excluding rubella infection is still very low in Poland. In 2014, only 0.6% of rubella cases were laboratory confirmed.

Measles in Poland in 2014

BACKGROUND: Since 1998, Poland has been actively participating in the Measles Elimination Program, coordinated by the World Health Organization (WHO). It requires achieving and maintaining very high vaccine coverage (>95%), recording all cases and suspected cases of measles, and laboratory testing of all suspected measles cases in the WHO Reference Laboratory. In Poland it is a Laboratory of Department of Virology, NIPHNIH. In order to confirm or exclude the case of measles specific measles IgM antibodies should be measured using Elisa test, or molecular testing (PCR) should be performed to detect the presence measles virus RNA in biological material. AIM: To assess epidemiological situation of measles in Poland in 2014, including vaccination coverage in Polish population, and Measles Elimination Program implementation status. METHODS: The descriptive analysis was based on data retrieved from routine mandatory surveillance system, measles case-based reports from 2014 sent to the Department of Epidemiology NIPH-NIH by Sanitary-Epidemiological Stations and data published in the annual bulletins "Infectious diseases and poisonings in Poland in 2014" and "Vaccinations in Poland in 2014" (MP Czarkowski et all., Warszawa 2015, NIZP-PZH, GIS). RESULTS: In total, there were 110 measles cases registered in Poland in 2014 (incidence 0.29 per 100,000), from which 87 cases (79%) were confirmed with laboratory test. That was more than in 2013 - when 84 cases were reported and incidence was 0,22. The highest incidence rate was observed among children aged 1 year (3,43 per 100,000). In 2014, 76 cases (69%) were hospitalized due to measles. No deaths from measles were reported. Vaccination coverage of children and youth aged 2-11 years ranged from 79.7% do 94.8% (primary vaccination in children born in 2004-2013) and from 77.7% to 85.8% (booster dose in children born in 2005-2011). In 2013, 127 measles-compatible cases were reported (67% of expected reports). In whole country the total number of suspects decreased form 258 in 2013 to 182 in 2014 r. SUMMARY AND CONCLUSIONS: In 2014, the epidemiological situation of measles deteriorated incomparison to proceeding year. The sensitivity of measles surveillance improved but is still insufficient. It is necessary to further promote Measles Elimination Program in Poland, to improve measles surveillance system and to maintain the high immunisation coverage.

Mumps in Poland in 2014

BACKGROUND: Vaccination against mumps from 2003 is mandatory in Poland and given as two dose scheme with MMR vaccine (mumps, measles, and rubella). Earlier this vaccination was only recommended. Despite observed decline in mumps incidence for over a decade which is a result of conducted vaccinations, mumps is still a common disease among the children. AIM: To assess epidemiological situation of mumps in Poland in 2014, including vaccination coverage in Polish population, in comparison to previous years. METHODS: The descriptive analysis was based on data retrieved from routine mandatory surveillance system and published in the annual bulletins "Infectious diseases and poisonings in Poland in 2014" and "Vaccinations in Poland in 2014" (1). Mumps cases were classified according to the criteria of surveillance case definition implemented in the European Union (Commission Decision of 28 April 2008 amending Decision 2002/253/EC). National Immunisation Programme for year 2014 was also used. RESULTS: In total, there were 2 508 mumps cases registered in Poland in 2014. Incidence of mumps was 6.5 per 100,000 and it was higher by 3.1 % in comparison with 2013 and lower by 9.7 % in comparison with median for the years 2008-2012. The highest incidence rate was observed among children aged 4 years (61.3 per 100,000). Incidence in men (7.8 per 100,000) was higher than in women (5.3). In 2014, 31 people were hospitalized due to mumps. Vaccination coverage of children aged 3 years in Poland in 2013 was 97.0% and it was lower by 0.5 % in comparison with year 2013 (97.5 %). CONCLUSIONS: Systematic execution of mumps vaccination in accordance with the National Immunisation Programme resulted in a significant decrease in the number of registered cases. Due to the high vaccination coverage further decline in the number of cases is expected.

Chickenpox in Poland in 2014

BACKGROUND: A large number of chickenpox cases, occurring especially in children between 0-14 years old and among those who are not vaccinated, indicates the rationale for the use of chickenpox vaccinations. In Poland since 2002, chickenpox vaccination is included in the National Immunisation Programme as recommended. AIM. To assess epidemiological situation of chickenpox in Poland in 2014 in comparison to previous years. AIM: To assess epidemiological situation of chickenpox in Poland in 2014 in comparison to previous years. METHODS: The descriptive analysis was based on data retrieved from routine mandatory surveillance system and published in the annual bulletins "Infectious diseases and poisonings in Poland in 2014" and "Vaccinations in Poland in 2014" (1;2). National Immunisation Programme for year 2014 was also used (3). RESULTS: In 2014, 221 628 cases of chickenpox were registered in Poland. The incidence was 575.9 and was lower than in 2013 (463.6). The highest number of cases was reported in mazowieckie voivodeship (35 321), the lowest in podlaskie voivodeship (5 346). The highest incidence was recorded in children aged 4 years. The chickenpox incidence among men was higher by 12.4% comparing to women (543.4). The incidence among rural residents (595.0) was higher by 9.8 % than among urban residents. Number of cases hospitalized due to mumps was 1 467. Number of people vaccinated against chickenpox was 63 608. SUMMARY: In 2014, there was increase in the incidence of chickenpox in Poland. Since 2002 the number of people vaccinated against chickenpox increased. The increase in the number of people vaccinated against chickenpox would help maintain the downward trend in subsequent years.

Deferoxamine improves antioxidative protection in the brain of neonatal rats: The role of anoxia and body temperature.

After hypoxic-ischemic insult iron deposited in the brain catalyzes formation of reactive oxygen species. Newborn rats, showing reduced physiological body temperature and their hyperthermic counterparts injected with deferoxamine (DF), a chelator of iron, are protected both against iron-mediated neurotoxicity and against depletion of low-molecular antioxidants after perinatal asphyxia. Therefore, we decided to study the effects of DF on activity of antioxidant enzymes (superoxide dismutase-SOD, glutathione peroxidase-GPx and catalase-CAT) in the brain of rats exposed neonatally to a critical anoxia at body temperatures elevated to 39°C. Perinatal anoxia under hyperthermic conditions intensified oxidative stress and depleted the pool of antioxidant enzymes. Both the depletion of antioxidants and lipid peroxidation were prevented by post-anoxic DF injection. The present paper evidenced that deferoxamine may act by recovering of SOD, GPx and CAT activity to reduce anoxia-induced oxidative stress.