Rotwein unter Hochspannung: Mehrjährige Qualitäts- Untersuchung mit Gas-Discharge-Visualisation (GDV)

We investigated whether we can detect any differences in red wines produced either by bio-dynamic or by standard organic agriculture. We used standard methods to investigate the quality of the wines and Gas-Discharge-Visualisation (GDV) method to investigate a holistic quality of the wines. With the GDV-method, samples are exposed to high voltage. The halo-like gas discharge caused by a burst of electron emission of the sample is captured by a digital camera underneath a transparent, dielectric surface. The wine samples measured originate from an On-Farm experiment in South of France with two separately managed but neighbouring blocks (same soil and climate conditions): bio-organic and bio-dynamic. Apart from the use of bio-dynamic preparations, plant protection and fertilization was the same in both blocks. The vinification of the sampled grapes was made in two replicates which were analysed separately. During the three years of examination, the bio-dynamic samples did not reveal significant differences when assessed with standard methods (sensory triangle test, polyphenol analysis etc.). However, with GDV measurements the values for the imageparameter “mean intensity” were mostly higher for the wines from bio-dynamically produced grapes. In a „mixed effect model“ (GDV-parameter „mean intensity“ as dependent variable, replication und cultivation-system as fix and year as random effect) the difference was statistically significant. We conclude that the GDV-method has an interesting potential to detect very sensitively differences in food attributes. However, in order to interpret the results in terms of consumer-relevant quality further research is needed

Роль мертвого пространства в формировании и диагностике дыхательной недостаточности

The volumes of the dead space (anatomic and alveolar) play an important role in the physiology of external respiration and information on these volumes makes the diagnosis of different respiratory disorders easier. The volume of the anatomic dead space (the last inspiratory portions) is uninvolved in the mixing with the gas of functional residual capacity (FRC) and leaves the airways unchanged in the gas composition on expiration. Mixing of the other portion of the tidal volume with FRC gas should be regarded as preparation for an alveolar gas exchange process. The increased partial value of the anatomic dead space in the tidal volume with its decrease (tachypnea) and, accordingly, reduced alveolar ventilation volume may result in ventilation respiratory failure. The time course of changes in the volume of the alveolar dead space is easily detectable from the decrease in expiratory CO2 concentrations as compared with PaCO2. The increased alveolar dead space volume suggests impaired local blood flow (thromboembolism, acute respiratory distress syndrome) in the lesser circulation and gives grounds to diagnose shunting and venous mixing. Procedures for measuring the dead space volumes are simple and may be introduced into clinical practice. Key words: anatomic dead space, alveolar dead space, functional residual capacity, respiratory failure.Объемы мертвого пространства (анатомического и альвеолярного) играют важную роль в физиологии внешнего дыхания, а информация об этих объемах и их динамике облегчает диагностику различных расстройств дыхания. Объем анатомического мертвого пространства — последние порции вдоха — не принимает участие в перемешивании с газом ФОЕ и уходит из дыхательных путей на выдохе в неизменном газовом составе. Перемешивание остальной части дыхательного объема с газом ФОЕ нужно считать подготовкой к процессу альвеолярного газообмена. Увеличение парциальной величины анатомического мертвого пространства в дыхательном объеме при его уменьшении (тахипноэ) и, соответственно, уменьшение объема альвеолярной вентиляции может привести к вентиляционной дыхательной недостаточности. Динамика объема альвеолярного мертвого пространства легко определяется по снижению концентрации СО2 в выдыхаемом воздухе по сравнению с РаСО2. Увеличение объема альвеолярного мертвого пространства свидетельствует о нарушении локального кровотока (тромбоэмболия, ОРДС) в системе малого круга кровообращения и дает основание для диагностики шунтирования и венозного примешивания. Методики измерения объемов мертвого пространства просты и могут быть внедрены в клиническую практику. Ключевые слова: анатомическое мертвое пространство, альвеолярное мертвое пространство, функциональная остаточная емкость, дыхательная недостаточность

Оптимизация проведения операционного периода при радикальных мастэктомиях

Blood loss volume is determined visually and approximately in most cases of surgical interventions, which most commonly leads to its underestimation, inadequate compensation, and development of hypovolemia. The latter induces peripheral vasospasm resulting in circulatory hypoxia, metabolic acidosis, diminished immunity, and worse reparative capacities of the body in the postoperative period. The transfused liquid volumes exceeding blood loss cause an increase in interstitial fluid volume, tissue edema and, hence, lead to impaired pulmonary gas exchange, enlarged postoperative wound edema, and postoperative complications. Administration of infusion media at a temperature lower than the body temperature has multiple adverse effects that impair the function of organs and systems. The typical response to hypothermia is peripheral vasospasm, followed by the development of circulatory hypoxia and metabolic acidosis. The objective of the study was to precisely estimate the volume of intraoperative blood loss and its adequate compensation and to correct central hemodynamic parameters and the body’s water sectors by nor-mothermal infusion therapy. Subjects and methods. The body’s water sectors, central hemodynamics, oxygen balance, and intraoperative blood loss volume were studied. Three groups of patients with radical mastectomy were comparatively analyzed. In Group 1 including 35 women operated on for breast cancer, the magnitude of blood loss was determined by eye and standard infusion therapy was performed, by using the mean solution temperatures of 20°C. Group 2 comprised 20 patients in whom blood loss was measured using a balance and infusion therapy was performed in accordance with the volume of the measured blood loss at the same temperature as in Group 1. Group 3 (n=18) received infusion therapy with the solutions warmed up to 37°C in accordance with blood loss volume determined applying a balance. Results. The studies have shown it necessary to monitor blood loss for its adequate compensation and to make appropriate correction of hemodynamic parameters along with normothermal infusion therapy during surgical interventions into the breast. Key words: monitoring of blood loss volume, the body’s water sectors, normothermal infusion therapy, central hemodynamics.В большинстве случаев оперативных вмешательств объем кровопотери определяют визуально и приблизительно, что чаще всего приводит к занижению объема кровопотери и к ее неадекватному возмещению и развитию гипо-волемии. Гиповолемия вызывает развитие спазма периферических сосудов, ведущего к циркуляторной гипоксии, метаболическому ацидозу, снижению иммунитета, с ухудшением репаративных возможностей организма в послеоперационном периоде. Если переливать объемы жидкостей, превышающие кровопотерю, то это приводит к увеличению объема интерстициальной жидкости, отеку тканей и, как следствие, к нарушению газообмена в легких, увеличению отека послеоперационной раны, развитию послеоперационных осложнений. Введение инфузи-онных сред с температурой ниже температуры тела вызывает в организме больного множество нежелательных эффектов, нарушающих функции органов и систем. Типичной реакцией на гипотермию является периферический вазоспазм с последующим развитием циркуляторной гипоксии и метаболического ацидоза. Нами поставлена цель точного определения объема операционной кровопотери и ее адекватное восполнение, коррекция параметров центральной гемодинамики и водных секторов организма с помощью нормотермической инфузионной терапии. Материал и методы. Изучали водные сектора организма, параметры центральной гемодинамики и кислородного баланса, объем операционной кровопотери. Сравнительный анализ проводили между тремя группами больных с радикальной мастэктомией. У 35 женщин (1-я группа), оперированных по поводу рака молочной железы, величину операционной кровопотери определяли «на глазок», и проводили стандартную инфузионную терапию со средней температурой растворов 20°С. Вторую группу (2-я) составили 20 пациенток, у которых крово-потерю измеряли весовым способом и проводили инфузионную терапию, в соответствии с объемом измеренной кровопотери и тем же температурным режимом, как и в 1-й группе). В третьей группе (18 человек) проводили ин-фузионную терапию согретыми до 37°С растворами в соответствии с объемом кровопотери, определяемым весовым способом. Результаты. Исследования показали необходимость мониторинга кровопотери для адекватного ее возмещения и соответствующей коррекции показателей гемодинамики, наряду с проведением нормотермиче-ской инфузионной терапии во время оперативных вмешательствах на молочной железе. Ключевые слова: мониторинг объёма кровопотери, водные сектора организма, нормотермическая инфузионная терапия, центральная гемодинамика

Targeted Deletion of Neuropeptide Y (NPY) Modulates Experimental Colitis

Neurogenic inflammation plays a major role in the pathogenesis of inflammatory bowel disease (IBD). We examined the role of neuropeptide Y (NPY) and neuronal nitric oxide synthase (nNOS) in modulating colitis.Colitis was induced by administration of dextran sodium sulphate (3% DSS) or streptomycin pre-treated Salmonella typhimurium (S.T.) in wild type (WT) and NPY (NPY(-/-)) knockout mice. Colitis was assessed by clinical score, histological score and myeloperoxidase activity. NPY and nNOS expression was assessed by immunostaining. Oxidative stress was assessed by measuring catalase activity, glutathione and nitrite levels. Colonic motility was assessed by isometric muscle recording in WT and DSS-treated mice.DSS/S.T. induced an increase in enteric neuronal NPY and nNOS expression in WT mice. WT mice were more susceptible to inflammation compared to NPY(-/-) as indicated by higher clinical & histological scores, and myeloperoxidase (MPO) activity (p<0.01). DSS-WT mice had increased nitrite, decreased glutathione (GSH) levels and increased catalase activity indicating more oxidative stress. The lower histological scores, MPO and chemokine KC in S.T.-treated nNOS(-/-) and NPY(-/-)/nNOS(-/-) mice supported the finding that loss of NPY-induced nNOS attenuated inflammation. The inflammation resulted in chronic impairment of colonic motility in DSS-WT mice. NPY -treated rat enteric neurons in vitro exhibited increased nitrite and TNF-alpha production.NPY mediated increase in nNOS is a determinant of oxidative stress and subsequent inflammation. Our study highlights the role of neuronal NPY and nNOS as mediators of inflammatory processes in IBD

Anti-Hu antibodies activate enteric and sensory neurons.

IgG of type 1 anti-neuronal nuclear antibody (ANNA-1, anti-Hu) specificity is a serological marker of paraneoplastic neurological autoimmunity (including enteric/autonomic) usually related to small-cell lung carcinoma. We show here that IgG isolated from such sera and also affinity-purified anti-HuD label enteric neurons and cause an immediate spike discharge in enteric and visceral sensory neurons. Both labelling and activation of enteric neurons was prevented by preincubation with the HuD antigen. Activation of enteric neurons was inhibited by the nicotinic receptor antagonists hexamethonium and dihydro-β-erythroidine and reduced by the P2X antagonist pyridoxal phosphate-6-azo (benzene-2,4-disulfonic acid (PPADS) but not by the 5-HT3 antagonist tropisetron or the N-type Ca-channel blocker ω-Conotoxin GVIA. Ca(++) imaging experiments confirmed activation of enteric neurons but not enteric glia. These findings demonstrate a direct excitatory action of ANNA-1, in particular anti-HuD, on visceral sensory and enteric neurons, which involves nicotinic and P2X receptors. The results provide evidence for a novel link between nerve activation and symptom generation in patients with antibody-mediated gut dysfunction

Hyaluronan Export through Plasma Membranes Depends on Concurrent K+ Efflux by Kir Channels

Hyaluronan is synthesized within the cytoplasm and exported into the extracellular matrix through the cell membrane of fibroblasts by the MRP5 transporter. In order to meet the law of electroneutrality, a cation is required to neutralize the emerging negative hyaluronan charges. As we previously observed an inhibiting of hyaluronan export by inhibitors of K+ channels, hyaluronan export was now analysed by simultaneously measuring membrane potential in the presence of drugs. This was done by both hyaluronan import into inside-out vesicles and by inhibition with antisense siRNA. Hyaluronan export from fibroblast was particularly inhibited by glibenclamide, ropivacain and BaCl2 which all belong to ATP-sensitive inwardly-rectifying Kir channel inhibitors. Import of hyaluronan into vesicles was activated by 150 mM KCl and this activation was abolished by ATP. siRNA for the K+ channels Kir3.4 and Kir6.2 inhibited hyaluronan export. Collectively, these results indicated that hyaluronan export depends on concurrent K+ efflux

Interleukin 2-regulated in vitro antibody production following a single spinal manipulative treatment in normal subjects

<p>Abstract</p> <p>Background</p> <p>Our recent investigations have demonstrated that cell cultures from subjects, who received a single spinal manipulative treatment in the upper thoracic spine, show increased capacity for the production of the key immunoregulatory cytokine, interleukin-2. However, it has not been determined if such changes influence the response of the immune effector cells. Thus, the purpose of the present study was to determine whether, in the same subjects, spinal manipulation-related augmentation of the <it>in vitro </it>interleukin-2 synthesis is associated with the modulation of interleukin 2-dependent and/or interleukin-2-induced humoral immune response (antibody synthesis).</p> <p>Methods</p> <p>A total of seventy-four age and sex-matched healthy asymptomatic subjects were studied. The subjects were assigned randomly to: venipuncture control (n = 22), spinal manipulative treatment without cavitation (n = 25) or spinal manipulative treatment associated with cavitation (n = 27) groups. Heparinized blood samples were obtained from the subjects before (baseline) and then at 20 minutes and 2 hours post-treatment. Immunoglobulin (antibody) synthesis was induced in cultures of peripheral blood mononuclear cells by stimulation with conventional pokeweed mitogen or by application of human recombinant interleukin-2. Determinations of the levels of immunoglobulin G and immunoglobulin M production in culture supernatants were performed by specific immunoassays.</p> <p>Results</p> <p>The baseline levels of immunoglobulin synthesis induced by pokeweed mitogen or human recombinant interleukin-2 stimulation were comparable in all groups. No significant changes in the production of pokeweed mitogen-induced immunoglobulins were observed during the post-treatment period in any of the study groups. In contrast, the production of interleukin-2 -induced immunoglobulin G and immunoglobulin M was significantly increased in cultures from subjects treated with spinal manipulation. At 20 min post-manipulation, immunoglobulin G synthesis was significantly elevated in subjects who received manipulation with cavitation, relative to that in cultures from subjects who received manipulation without cavitation and venipuncture alone. At 2 hr post-treatment, immunoglobulin M synthesis was significantly elevated in subjects who received manipulation with cavitation relative to the venipuncture group. There were no quantitative alterations within the population of peripheral blood B or T lymphocytes in the studied cultures.</p> <p>Conclusion</p> <p>Spinal manipulative treatment does not increase interleukin-2 -dependent polyclonal immunoglobulin synthesis by mitogen-activated B cells. However, antibody synthesis induced by interleukin-2 alone can be, at least temporarily, augmented following spinal manipulation. Thus, under certain physiological conditions spinal manipulative treatment might influence interleukin-2 -regulated biological responses.</p

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus : implications for seizure susceptibility

Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55(-/-) mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subunits while GluR1, GluR2, GluR6/7 and NR2A/B were unchanged as compared to wild-type mice. In p75(-/-) mice, GluR2, GluR3, GluR6/7 and NR2A/B glutamate receptor subunits were increased in the hippocampus while GluR1 and NR1 did not change. Extracellular single-cell recordings of the electrical activity of hippocampal neurons were carried out in anesthetized mice by standard electrophysiological techniques. Microiontophoretic application of glutamate increased the basal firing rate of hippocampal neurons in p75(-/-) mice versus wild-type mice, and this effect was blocked by 2-amino-5-phosphopentanoic acid and 6-nitro-7-sulfamoyl-benzo(f)quinoxaline-2,3-dione denoting the involvement of N-methyl-D-aspartic acid and AMPA receptors. In p55(-/-) mice, hippocampal neurons responses to glutamate were similar to wild-type mice. Spontaneous glutamate release measured by in vivo hippocampal microdialysis was significantly decreased only in p55(-/-) mice. No changes were observed in KCl-induced glutamate release in both receptor knockout mice strains versus wild-type mice. These findings highlight specific molecular and functional interactions between p55 and p75 receptor-mediated signaling and the glutamate system. These interactions may be relevant for controlling neuronal excitability in physiological and pathological conditions.peer-reviewe