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WstępCholecystokinina (CCK) należy do hormonów peptydowych układu pokarmowego regulujących trawienie lipidów i białek, a ponadto jest ośrodkowym neurotransmiterem/neuromodulatorem. Po podaniu dożylnym wywołuje efekt resuscytacyjny u szczurów we wstrząsie krwotocznym. Ze względu na fakt, iż CCK może wpływać bezpośrednio i pośrednio na czynność ośrodka sercowo-naczyniowego, celem pracy było zbadanie działania pochodnej siarczanowej oktapeptydu CCK (CCK-8) podawanej do komory bocznej mózgu (intracerebroventricularly – icv) w fazie hamowania czynności układu współczulnego we wstrząsie krwotocznym.Materiał i metodyBadania przeprowadzono u samców szczurów szczepu Wistar w znieczuleniu ogólnym (ketamina [100 mg/kg]/ksylazyna [10 mg/kg]), u których wywołano nieodwracalny wstrząs krwotoczny (0% przeżycia 2 h) ze średnim ciśnieniem tętniczym (mean arterial pressure – MAP) 20–25 mmHg. W 5 min krytycznej hipotensji szczurom podawano icv CCK-8 (5, 15 nmol) lub 0,9% roztwór NaCl (5 μl).WynikiKrwotok prowadził do obniżenia ciśnienia tętna (pulse pressure – PP), częstości rytmu serca (heart rate – HR) oraz wzrostu nerkowego (renal vascular resistance – RVR) i krezkowego oporu naczyniowego (mesenteric vascular resistance – MVR). W grupie kontrolnej nie stwierdzono wzrostu badanych parametrów układu krążenia, a średni czas przeżycia wynosił 32,5 ± 5,1 min. CCK-8 wywoływała zależne od dawki spadki MAP, PP i HR ze wzrostem RVR i MVR, a także skracała czas przeżycia w porównaniu ze zwierzętami kontrolnymi.WnioskiOśrodkowo działająca CCK-8 wywołuje działanie depresyjne na układ krążenia u szczurów we wstrząsie krwotocznym.

Wstęp:Pobudzenie ośrodkowego układu histaminergicznego wywołuje działanie resuscytacyjne u szczurów we wstrząsie krwotocznym. Skoro podawana dożylnie bombezyna wykazuje podobne działanie, a receptory bombezynowe są obecne w strukturach ośrodkowego układu nerwowego, odpowiedzialnych za regulację czynności układu krążenia, celem pracy było zbadanie wpływu zablokowania receptorów bombezynowych na efekty krążeniowe wynikające z podania do komory bocznej mózgu (icv) histaminy we wstrząsie krwotocznym u szczurów.Materiał i metody:Badania przeprowadzono u szczurów, samców szczepu Wistar w znieczuleniu ogólnym (ketamina 100 mg/kg + ksylazyna 10 mg/kg, dootrzewnowo). Zastosowano model odwracalnego wstrząsu krwotocznego ze średnim ciśnieniem tętniczym (MAP) 30–35 mmHg. Niezwłocznie po zakończeniu krwawienia podawano icv antagonistów receptorów bombezynowych/0,9% roztwór NaCl, a 5 min później tą samą drogą histaminę (50 nmol) bądź 0,9% roztwór NaCl.Wyniki:Utrata krwi prowadziła do obniżenia ciśnienia tętna (PP), częstości rytmu serca (HR) i przepływu krezkowego krwi (MBF). Histamina wywoływała działanie presyjne ze wzrostem PP i MBF. Efekty działania histaminy były częściowo hamowane przez [D-Phe12,Leu14]-bombezynę i BIM 23042, odpowiednio nieselektywnego antagonistę receptorów bombezynowych oraz selektywnego blokera receptorów bombezynowych typu 1 (BB1). W grupach kontrolnych nie stwierdzono wpływu antagonistów receptorów bombezynowych na mierzone parametry układu krążenia.Wnioski:Endogenne peptydy bombezynopodobne, działając poprzez receptory BB1, mogą wpływać na wywoływane przez ośrodkowo działającą histaminę działanie resuscytacyjne we wstrząsie krwotocznym u szczurów.

The survival of erythrocytes in the circulating blood depends on their membranes’ structural and functional integrity. One of the mechanisms that may underlie the process of joint degeneration is the imbalance of prooxidants and antioxidants, promoting cellular oxidative stress. The study is aimed at observing the effects of the 21-day general rehabilitation program on the erythrocytes redox status and serum ST2 marker in patients after knee or hip replacement in the course of osteoarthritis. Erythrocytes and serum samples were collected from 36 patients. We analyzed the selected markers of the antioxidant system in the erythrocytes: catalase (CAT), glutathione reductase (glutathione disulfide reductase (GR, GSR)), total superoxide dismutase activity (SOD), glutathione peroxidase (GPx), glutathione transferase (GST) activity, and cholesterol and lipofuscin (LPS) concentration. In serum, we analyzed the concentration of the suppression of tumorigenicity 2 (ST2) marker. After the 21-day general rehabilitation program, the total SOD and GPx activity, measured in the hemolysates, significantly increased ( p < 0.001 ) while LPS, cholesterol, and ST2 levels in serum significantly decreased ( p < 0.001 ). General rehabilitation reduces oxidative stress in patients after knee or hip replacement in the course of osteoarthritis. Individually designed, regular physical activity is the essential element of the postoperative protocol, which improves the redox balance helping patients recover after the s4urgery effectively.

Since biological applications and toxicity of graphene-based materials are structure dependent, studying their interactions with the biological systems is very timely and important. We studied short-term (1, 24, and 48 h) effects of ultrapure (GO) and Mn2+-contaminated (GOS) graphene oxide on normal human dermal fibroblasts (NHDF) and adenocarcinomic human alveolar basal epithelial cells (A549) using selected oxidative stress markers and cytokines: glutathione reductase (GR) and catalase (CAT) activity, total antioxidative capacity (TAC), and malondialdehyde (MDA) concentration, levels of vascular endothelial growing factor (VEGF), tumor necrosis factor-alpha (TNF-α), platelet-derived growth factor-BB (PDGF-BB), and eotaxin. GOS induced higher levels of oxidative stress, measured with CAT activity, TAC, and MDA concentration than GO in both cell lines when compared to control cells. GR activity decreased in time in NHDF cells but increased in A549 cells. The levels of cytokines were related to the exposure time and graphene oxide type in both analyzed cell lines and their levels comparably increased over time. We observed higher TNF-α levels in NHDF and higher levels of VEGF and eotaxin in the A549 cell line. Both types of cells showed similar susceptibility to GO and GOS. We concluded that the short-time exposure to GOS induced the stronger response of oxidative stress markers without collapsing the antioxidative systems of analysed cells. Increased levels of inflammatory cytokines after GO and GOS exposure were similar both in NHDF and A549 cells.

Metabolic surgery ameliorates insulin resistance and is associated with long-term, effective weight loss, but the mechanisms involved remain unknown. Here, the duodenal-jejunal omega switch (DJOS) surgery in combination with high-fat, high-carbohydrate diet was performed on diet obese rats and joint effects of bariatric surgery and different dietary patterns on heat shock protein 70 (HSP70) and HSP90 plasma and liver concentrations were measured. We found that plasma and liver levels of HSP70 were lower after DJOS surgery in comparison to the control in the groups of animals kept on control diet (CD) and high-fat, high-sugar diet (HFS) but the postoperative change of the diet led to the increase in HSP70 in plasma and liver concentration in DJOS-operated animals. A high-calorie meal, rich in carbohydrates and fats, significantly increased circulating levels of HSP90, reducing the normalising effect of DJOS. The HFS diet applied during all stages of the experiment led to the higher levels of liver HSP90 concentration. The combination of CD and DJOS surgery was the most efficient in the lowering of the HSP90 liver concentration. The normalisation of circulating levels and liver concentrations of HSP70 and HSP90 may be achieved in a combination of DJOS procedure with a proper dietary plan.

We studied the long-term effect of ileal transposition (IT) metabolic surgery on the hepatokines: retinol-binding protein-4 (RBP4), α-2-HS-glycoprotein (aHSG/fetuin-A), and fibroblast growth factor 21 (FGF21), C-reactive protein (CRP) plasma levels, glucose metabolism, body weight, liver histology, as well as total lipids concentration in muscle, liver, and fat tissue of obese Zucker (Crl:ZUC(ORL)-Leprfa) rats. 14 adult males were randomly submitted either to IT or SHAM (control) surgery. Pre-operative hepatokines plasma levels were not significantly different in rats submitted to IT or SHAM protocol. Three months after the procedures the plasma levels of RBP4, aHSG, FGF21, and CRP were significantly lower in IT-operated animals when compared to SHAM-operated group. Three and 12 weeks after the IT and SHAM surgery, the AUCOGTT were significantly lower than AUCOGTT before the surgery. HOMA-IR was lower in rats after IT surgery in comparison to the SHAM-operated rats. Muscle and liver total lipids concentration was reduced after the IT procedure when compared to pre-IT conditions. IT had a significant reductive impact on the body weight in comparison to SHAM surgery in the 4th, 6th, 8th, and 10th week after the surgery. We conclude that IT reduces hepatokines’ plasma concentrations, muscle and liver total lipids concentration but not the inflammatory processes in the liver of Zucker (Crl:ZUC(ORL)-Leprfa) rats.

Background. Metabolic surgery procedures are designed not only for sustained weight loss but also for achieving positive metabolic changes, including improved glucose tolerance and insulin sensitivity, along with an increase in energy expenditure. Based on recent findings, the present study focuses on the relationship between the effects of ileal transposition (IT), high-fat diet (HFD), and selected markers of lipid metabolism and inflammation. Methods. Forty-eight male rats were divided into two groups: HFD and control diet (CD) fed rats. After eight weeks, animals in each group were randomly assigned to two types of surgery: IT and SHAM. Thereafter, fifty percent of the animals in the HFD and CD groups had their diets changed, while the remaining half maintained their presurgery diets. Eight weeks after surgery, plasma levels of ANGPTL8, PTX3, leptin, and adiponectin were assessed. Results. The IT group pre- and postoperatively maintained on the HFD showed higher ANGPTL8 level compared to SHAM operated animals ( p = 0.0041 ). The effect of IT on PTX3 level in the group pre- and postoperatively maintained on a CD was not significant, and there were no differences compared to SHAM. Only the postoperative diet change to HFD increased PTX3 level in the IT operated animals ( p = 0.0002 ). The IT group had increased plasma adiponectin ( p = 0.026 ) and leptin ( p = 0.0027 ) levels after dietary change to HFD compared to IT rats fed CD. Conclusions. This study indicates that the outcomes of metabolic surgery can be greatly modified by HFD. The effects of the IT procedure in this experiment are ambiguous and do not provide a clear answer as to whether or not they are beneficial.

Imbalance in prooxidant-antioxidant equilibrium plays an important role in the progression of osteoarthritis (OA). Postoperative rehabilitation significantly improves the functional activity of patients with OA. We aimed to assess the effect of the general 21-day postoperative rehabilitation on the oxidative stress markers in patients after total hip arthroplasty or knee replacement. Patients (n =41) started individually designed postoperative rehabilitation ca. 90 days after endoprosthesis implantation. We used the six-minute walk test (6MWT) to quantify the changes in their exercise capacity. We analyzed the oxidative stress markers: total antioxidant capacity (TAC), total superoxide dismutase (SOD), Cu-Zn-superoxide dismutase (CuZnSOD) and ceruloplasmin (Cp) activity, malondialdehyde (MDA) and lipofuscin (LPS) concentration in patients serum to asses changes in the oxidative stress intensity. We found that after 21-days postoperative rehabilitation program: the average distance walked by patients increased by 69 m; TAC increased by 0.20 ± 0.14 mmol/l; both SOD isoforms activities increased by 1.6 (±1.7) and 1.72 (±1.5) NU/ml, respectively; but Cp activity decreased by 1.8 (0.7-3.7) mg/dl. Also, we observed lower concentrations of lipid peroxidation markers: by 19.6 ± 24.4 μmol/l for MDA and by 0.4 ± 0.5 RF for LPS. A 21-day postoperative rehabilitation program effectively reduces oxidative processes, which helps the patients after total hip or knee replacement in a successful recovery.

WstępPobudzenie ośrodkowego układu histaminergicznego wywołuje działanie resuscytacyjne w modelu wstrząsu krwotocznego, podczas gdy neuropeptyd Y (NPY) podawany do komory bocznej mózgu (icv) powoduje efekt depresyjny w stanie hipotensji krwotocznej. Mając na uwadze, iż na neurony histaminergiczne jądra guzowo-suteczkowatego mają wpływ neurony wytwarzające NPY zlokalizowane w jądrze olbrzymiokomórkowym tylnym podwzgórza, celem pracy było zbadanie (1) efektów krążeniowych antagonisty receptorów typu 1 dla NPY (Y1) we wstrząsie krwotocznym oraz (2) możliwego udziału układu histaminergicznego w tych efektach.Materiał i metodyBadania przeprowadzono u szczurów samców szczepu Wistar w znieczuleniu ogólnym przy użyciu ketaminy i ksylazyny, u których wywoływano nieodwracalny wstrząs krwotoczny ze średnim ciśnieniem tętniczym (MAP) 20–25 mmHg oraz wskaźnikiem przeżycia 2 h 0%. Niezwłocznie po indukcji wstrząsu dokonywano pre-medykacji icv antagonistami receptorów histaminowych H1 i H2 chlorfenyraminą (50 nmol) i ranitydyną (50 nmol), antagonistą/odwrotnym agonistą receptorów H3/4 tioperamidem bądź 0,9% roztworem NaCl. Po pięciu minutach zwierzętom podawano icv antagonistę receptorów Y1 BIBP 3226 (64 nmol/kg).WynikiBIBP 3226 wywoływał wzrosty MAP, ciśnienia tętna (PP) oraz nerkowego przepływu krwi (RBF), powodował także wzrost do 100% wskaźnika przeżycia 2 h. Chlorfenyramina hamowała zmiany MAP, PP i RBF wywoły-wane przez BIBP 3226 oraz zmniejszała do 0% wskaźnik przeżycia 2 h. W odróżnieniu do tego ranitydyna i tioperamid nie wykazywały wpływu na działanie BIBP 3226.WnioskiZablokowanie ośrodkowych receptorów Y1 wywołuje efekt presyjny u szczurów we wstrząsie krwotocznym. Działanie to odbywa się przy udziale układu histaminergicznego.

Retinopathy of prematurity belongs to the group of proliferative retinopathies. It affects preterm infants with very low birth weight, treated with high concentrations of oxygen. It is estimated that retinopathy of prematurity leads to blindness in approximately 50,000 children per year worldwide. There were two epidemics of retinopathy of prematurity in the 50s and 70s of the last century. Another increase in the incidence, referred to as the third epidemic in the literature, has been observed in recent years in developing countries. So far, high oxygen concentrations used in adjuvant oxygen therapy have been considered to be the major risk factor for retinopathy of prematurity. There are, however, reports on the development of the disease in patients who received no oxygen therapy. Low birth weight and early gestational age are well-known risk factors for retinopathy of prematurity. Other important risk factors include sex, multiple pregnancy, intraventricular haemorrhage and blood transfusions. The disease can be prevented by screening performed by an ophthalmologist within a few weeks after birth. Laser retinal photocoagulation, which is primarily aimed to inhibit fibrovascular proliferation, is the standard therapy in infants with retinopathy of prematurity. Surgical treatment is necessary in the case of disease progression despite laser photocoagulation. Attempts are also made to use vascular endothelial growth factor blockers. The aim of the paper is to present the pathomechanism and the main factors involved in the development of retinopathy of prematurity as well as the current therapeutic approaches for this disease. This information is intended to help family doctors update their knowledge on retinopathy of prematurity.

BACKGROUND A number of studies have documented the influence of cigarette smoking on hearing. However, the association between sex and hearing impairment in smokers as measured by otoacoustic emissions (OAEs) has not been clearly established. The aim of this study was to analyze sex-specific effects of smoking on hearing via conventional and ultra-high-frequency pure tone audiometry (PTA), and OAEs, specifically spontaneous OAEs, click-evoked OAEs, and distortion-product OAEs. MATERIAL AND METHODS The study included 84 healthy volunteers aged 25-45 years (mean 34), among them 46 women (25 non-smokers and 21 smokers) and 38 men (16 non-smokers and 22 smokers). The protocol of the study included otoscopic examination, tympanometry, low-, moderate-, and ultra-high-frequency PTA, evaluation of spontaneous click-evoked (CEAOEs) and distortion-product otoacoustic emissions (DPOAEs), assessment of the DP-grams for 2f1-f2 (f1 from 977 to5 164 Hz), and input/output function at L2 primary tone level of 40-70 dB SPL. RESULTS Smokers and non-smokers did not differ significantly in terms of their hearing thresholds assessed with tone audiometry. Male smokers presented with significantly lower levels of CEAOEs and DPOAEs than both male non-smokers and female smokers. CONCLUSIONS Smoking does not modulate a hearing threshold determined with PTA at low, moderate, and ultra-high frequencies, but causes a significant decrease in OAE levels. This effect was observed only in males, which implies that they are more susceptible to smoking-induced hearing impairment. Sex-specific differences in otoacoustic emissions level may reflect influences of genetic, hormonal, behavioral, and/or environmental factors.

Sery należą do produktów o wysokiej zawartości tłuszczu, białka i innych związków nieorganicznych. Są wyrobem spożywczym, który może różnić się jednostkowo w zależności od swojego pochodzenia, warunków wytwarzania, flory mikrobiologicznej i aktywności enzymatycznej. Wszystkie te parametry mogą oddziaływać na skuteczność analityczną, w konsekwencji stanowiąc utrudnienie w oznaczaniu stężenia histaminy w serach. Do głównych czynników wpływających na powstawanie w produktach spożywczych amin biogennych, w tym histaminy, należą: obecność bakterii (LAB), kultury starterowe, dostępność wolnych aminokwasów, okres dojrzewania sera, aktywność proteolityczna, pH, temperatura i stężenie NaCl. Nie wykazano korelacji pomiędzy niekorzystnymi skutkami a zawartością amin w żywności. Można przypuszczać, że stężenie histaminy powyżej 100 mg/kg w produktach spożywczych nie jest zalecane. Dzięki ścisłym reżimom technologicznym podczas produkcji żywności częstość zatruć pokarmowych histaminą, wynikających z zanieczyszczeń bakteryjnych, jest sporadyczna.

WstępReceptory histaminowe H3 występują w ośrodkowym i obwodowym układzie nerwowym, w tym na zakończeniach pozazwojowych układu współczulnego. Działają głównie jako presynaptyczne auto- i heteroreceptory, są odpowiedzialne za regulację syntezy oraz wydzielania histaminy i innych neurotransmiterów/neuromodulatorów. Celem pracy było zbadanie wpływu zablokowania receptorów H3 na czynność układu krążenia podczas fazy hamowania aktywności układu współczulnego w modelu wstrząsu krwotocznego u szczurów.Materiał i metodyBadania przeprowadzono u szczurów samców szczepu Wistar, w znieczuleniu ogólnym przy użyciu ketaminy i ksylazyny (100 mg/kg + 10 mg/kg dootrzewnowo), u których wywołano nieodwracalny wstrząs krwotoczny ze średnim ciśnieniem tętniczym (MAP) 20-25 mmHg (wskaźnik przeżycia 2 h: 0%). W 5 min krytycznej hipotensji zwierzętom podawano dożylnie antagonistę receptorów H3 JNJ 5207852 bądź 0,9% roztwór NaCl.WynikiKrwotok prowadził do obniżenia ciśnienia tętna (PP) i częstości rytmu serca (HR). JNJ 5207852 (1 i 5 mg/kg) wywoływał długotrwałe wzrosty MAP, PP i HR, a także zwiększenie do 100% wskaźnika przeżycia 2 h (5 mg/kg). Chemiczna sympatektomia wykonana przy użyciu 6-hydroksydopaminy (50 mg/kg przez trzy kolejne dni) hamowała zmiany MAP, PP i HR wywoływane przez JNJ 5207852 (5 mg/kg) i zmniejszała do 0% wskaźnik przeżycia 2 h.WnioskiAntagonista receptorów histaminowych H3 JNJ 5207852 wywołuje efekt resuscytacyjny u szczurów we wstrząsie krwotocznym, a jego mechanizm działania związany jest z aktywnością pozazwojowych neuronów układu współczulnego.

Background The benefits of IT surgery are based on incretin effects. In this study we show the influence of high fat diet (HFD) used both before and after surgery, on ileal transposition (IT) effects. Methods Forty-eight male rats were assigned to two groups: HFD and control diet (CD) fed rats. After eight weeks, HFD and CD fed rats were randomly assigned to two types of surgery: IT and SHAM, then for 50% of animals of each group the diet was changed, whereas the other 50% received the same type of diet. Eight weeks after surgery the incretin level, glucose tolerance as well as body mass and insulin level were assessed. Results GLP-1 plasma concentration was significantly higher in the IT operated CD/CD group compared to fasting state and did not differ significantly from the SHAM operated CD/CD animals. IT influenced the glucose stimulated PYY plasma level when compared with SHAM operated animals in the CD/HFD group, where the PYY plasma level was higher than in the SHAM operated animals. The effect of IT as well as of pre and postoperative diet on GIP plasma levels were insignificant. The IT group members maintained on the CD were characterised by a lower fasting glucose level, both pre and postoperatively, compared with the SHAM operated animals. The effect of IT on the fasting glucose level in groups preoperatively maintained on an HFD was insignificant. Conclusions IT surgery itself seems to have rather limited incretin effects in rats, whose obesity is the result of HFD.

Purpose. To study the effect of duodenal-jejunal omega switch (DJOS) in combination with different dietary patterns on the retinol-binding protein (RBP4), fetuin-A, and fibroblast growth factor 21 (FGF21) plasma levels and their hepatic gene expressions in rats. Methods. A high-fat diet (HF) was given to 28 rats and 28 more were fed with a control diet (CD) for 2 months. After that, half of each group underwent either DJOS or SHAM surgery. For the next 2 months, half of the animals in each operation group were kept on the same diet as before and half of them had the diet changed. After 16 weeks of the experiment RBP4, fetuin-A, and FGF21 plasma levels as well as liver Rbp4, Ahsg, and Fgf21 gene expressions were measured. Results. DJOS had a reductive impact on plasma levels of RBP4, fetuin-A, and FGF21 and Rbp4, Ahsg, and Fgf21 relative gene expression in the liver when compared to SHAM. The HF/HF group expressed significantly higher RBP4 and fetuin-A plasma levels in comparison to the control. The HF diet used before and/or after surgery led to upregulation of Rbp4, Ahsg, and Fgf21 relative gene expression. The lowest levels of analyzed parameters were observed in the CD/CD group. Conclusions. The efficiency of DJOS surgery, measured by hepatokines’ plasma levels and their gene expressions in the liver, depends on the type of diet applied before and after surgery. Manipulation of dietary patterns can lead to marked improvements in metabolic profile after DJOS surgery.

WstępLeptyna podawana do komory bocznej mózgu (icv) wywołuje efekt resuscytacyjny u szczurów we wstrząsie krwotocznym; w działaniu tym uczestniczy układ histaminergiczny. Celem obecnej pracy było zbadanie możliwego udziału receptorów histaminowych H3 w wywoływanym przez leptynę wpływie na układ krążenia we wstrząsie.Materiał i metodyBadania przeprowadzono u szczurów, samców szczepu Wistar w znieczuleniu ogólnym przy użyciu ketaminy i ksylazyny (100 mg/kg + 10 mg/kg dootrzewnowo), u których wywołano nieodwracalny wstrząs krwotoczny ze średnim ciśnieniem tętniczym (MAP) 20–25 mmHg (wskaźnik przeżycia dwugodzinnego: 0%). W 5 min krytycznej hipotensji zwierzętom podawano icv leptynę (20 µg) bądź 0,9% roztwór NaCl (5 µl).WynikiUtrata krwi prowadziła do obniżenia ciśnienia tętna (PP) i częstości rytmu serca (HR). Leptyna wywoływała długotrwałe wzrosty MAP, PP i HR, a także podwyższenie do 100% wskaźnika przeżycia dwugodzinnego. Premedykacja odwrotnym agonistą receptorów H3/częściowym agonistą receptorów H4 klobenpropitem (42,5 nmol, icv), ale nie neutralnym antagonistą receptorów H3 VUF 5681 (50 nmol, icv), hamowała zmiany MAP i PP wywoływane przez leptynę, jednak bez wpływu na wskaźnik przeżycia dwugodzinnego we wstrząsie.WnioskiReceptory histaminowe H3 mogą wpływać na efekt resuscytacyjny wywoływany przez ośrodkowo działającą leptynę we wstrząsie krwotocznym u szczurów.

Histamine, acting centrally as a neurotransmitter, evokes a reversal of hemorrhagic hypotension in rats due to the activation of the sympathetic and the renin–angiotensin systems as well as the release of arginine vasopressin and proopiomelanocortin-derived peptides. We demonstrated previously that central nicotinic cholinergic receptors are involved in the pressor effect of histamine. The aim of the present study was to examine influences of centrally administrated histamine on acetylcholine (ACh) release at the posterior hypothalamus—a region characterized by location of histaminergic and cholinergic neurons involved in the regulation of the sympathetic activity in the cardiovascular system—in hemorrhage-hypotensive anesthetized rats. Hemodynamic and microdialysis studies were carried out in Sprague–Dawley rats. Hemorrhagic hypotension was induced by withdrawal of a volume of 1.5 ml blood/100 g body weight over a period of 10 min. Acute hemorrhage led to a severe and long-lasting decrease in mean arterial pressure (MAP), heart rate (HR), and an increase in extracellular posterior hypothalamic ACh and choline (Ch) levels by 56% and 59%, respectively. Intracerebroventricularly (i.c.v.) administered histamine (50, 100, and 200 nmol) dose- and time-dependently increased MAP and HR and caused an additional rise in extracellular posterior hypothalamic ACh and Ch levels at the most by 102%, as compared to the control saline-treated group. Histamine H1 receptor antagonist chlorpheniramine (50 nmol; i.c.v.) completely blocked histamine-evoked hemodynamic and extracellular posterior hypothalamic ACh and Ch changes, whereas H2 and H3/H4 receptor blockers ranitidine (50 nmol; i.c.v.) and thioperamide (50 nmol; i.c.v.) had no effect. In conclusion, centrally administered histamine, acting via H1 receptors, increases ACh release at the posterior hypothalamus and causes a pressor and tachycardic response in hemorrhage-hypotensive anesthetized rats.

Langerhans cell histocytosis is a rare disease. LCH is reported mainly in children aged less than 15 years, however it may appear at any age. In this work, the case of 17-month boy is reported. The boy was admitted to the pediatric ophthalmology department in order to diagnose the swelling and bruising in the lower part of left orbit, which had lasted for one month before. The clinical status, various imaging techniques' results (MRI, TK and PET) and immunohistochemistry led to the final diagnosis of multisystem LCH (spread to masticator muscle and zygomatic bone). After the pharmacological therapy the total remission was achieved. Since four years the child is regularly controlled by oncologists and hematologists with no relapse reported.

Melanocortin peptides induce neuroprotection in acute and chronic experimental neurodegenerative conditions. Melanocortins likewise counteract systemic responses to brain injuries. Furthermore, they promote neurogenesis by activating critical signaling pathways. Melanocortin-induced long-lasting improvement in synaptic activity and neurological performance, including learning and memory, sensory-motor orientation and coordinated limb use, has been consistently observed in experimental models of acute and chronic neurodegeneration. Evidence indicates that the neuroprotective and neurogenic effects of melanocortins, as well as the protection against systemic responses to a brain injury, are mediated by brain melanocortin 4 (MC4) receptors, through an involvement of the vagus nerve. Here we discuss the targets and mechanisms underlying the multiple beneficial effects recently observed in animal models of neurodegeneration. We comment on the potential clinical usefulness of melanocortin MC4 receptor agonists as neuroprotective and neuroregenerative agents in ischemic stroke, subarachnoid hemorrhage, traumatic brain injury, spinal cord injury, and Alzheimer's disease.

Background Overexpression and enhanced release of vascular endothelial growth factor (VEGF) have been detected in various types of allergic inflammation, including asthma. Aim To further evaluate the pattern of systemic release of VEGF in atopic allergy, free circulating VEGF was measured in patients with persistent allergic rhinitis (PAR). Methods The concentrations of VEGF and its soluble receptors (sVEGF-R1 and VEGF-R2) in plasma were measured in patients with PAR sensitized to house dust mites and the healthy subjects. Results No significant differences were found between PAR patients and healthy subjects with respect to plasma levels of VEGF and its receptors. Conclusions It seems that free circulating VEGF may not be elevated in PAR patients. Moreover, on the basis of the present study as well as the earlier ones, it appears likely that systemic release of VEGF varies among patients with distinct clinical manifestation of atopy; may depend on severity/activity and the extent of inflammatory response.

LIGHT (homologous to lymphotoxins, exhibiting inducible expression, and competing with herpes simplex virus (HSV) glycoprotein D for herpes virus entry mediator (HVEM), a receptor expressed by T lymphocytes) has been involved in various autoimmune and inflammatory disorders. LIGHT induces the expression of interleukin-8 (IL-8), which is up-regulated in chronic spontaneous urticaria (CSU). To determine circulating soluble LIGHT concentration and its relationship with IL-8 concentration in patients with CSU. Concentrations of LIGHT, IL-8, and C-reactive protein (CRP) were determined in plasma or serum of CSU patients by an enzyme-linked immunosorbent assay. LIGHT plasma concentration was significantly higher in moderate–severe CSU patients as compared with the healthy subjects, but not with mild CSU patients. There were significant correlations between increased LIGHT and IL-8 concentrations, but not with increased CRP in CSU patients. Enhanced plasma concentrations of soluble LIGHT and its association with IL-8 concentration suggest the role of LIGHT in systemic inflammatory activation in CSU patients. We hypothesize that LIGHT-mediated immune–inflammatory response plays a role in severe phenotypes of the disease.

Melanocortin peptides induce neuroprotection in acute and chronic experimental neurodegenerative conditions. Melanocortins likewise counteract systemic responses to brain injuries. Furthermore, they promote neurogenesis by activating critical signaling pathways. Melanocortin-induced long-lasting improvement in synaptic activity and neurological performance, including learning and memory, sensory-motor orientation and coordinated limb use, has been consistently observed in experimental models of acute and chronic neurodegeneration. Evidence indicates that the neuroprotective and neurogenic effects of melanocortins, as well as the protection against systemic responses to a brain injury, are mediated by brain melanocortin 4 (MC