Aromatase and estrogen receptor beta expression in the rat olfactory bulb: neuroestrogen action in the first relay station of the olfactory pathway?

The expression pattern of aromatase (ARO), the enzyme converting androgens to estrogens, was analyzed in the olfactory bulb of adult male rats and was compared with the distribution of estrogen receptor beta (ER beta), the main estrogen receptor isoform expressed in this brain region. A strong ARO immunolabeling obtained with a specificity tested antibody was observed in juxtaglomerular neurons of the glomerular layer and a weaker immunoreaction was detected in the mitral cell layer of the main olfactory bulb, while the granule cell layer of the main olfactory bulb as well as all layers in the accessory olfactory bulb showed faint immunolabeling. Fluorescence double labeling experiments revealed that ARO detected in juxtaglomerular neurons of the main olfactory bulb colocalized with tyrosine hydroxylase (TH) and glutamic acid decarboxylase 67 (GAD67), while no colocalization between ARO and the calcium binding proteins calretinin (CR) and calbindin (CB) was observed. Furthermore, the TH immunoreactive neurons expressed metabotropic glutamate receptor 1 (mGluR1) too. ER beta immunoreactivity, in contrast to ARO, was detected in all layers of both the main and accessory olfactory bulb. In the glomerular layer of the main olfactory bulb it was expressed in TH and GAD67 containing juxtaglomerular neurons, and it colocalized with CR, CB and even with glial fibrillary acidic protein too. Our morphological findings suggest that ARO expression is a novel feature of dopaminergic/GABAergic juxtaglomerular neurons in the adult rat main olfactory bulb, and raise the possibility that ARO activity may change in function of olfactory input via mGluR1. In situ estrogen production in the olfactory bulb in turn may modulate interglomerular circuits through ER beta

Fe microenvironments in heat treated rare-earth exchanged montmorillonites

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A kardiológiai rehabilitáció teljesítménymutatói Magyarországon = Performance indicators of cardiac rehabilitation in Hungary

Absztrakt Bevezetés: Az akut kardiológiai események túlélésének javulásával, az életkor kitolódásával egyre nagyobb igény mutatkozik a kardiológiai rehabilitációs ellátásokra. Célkitűzés: Elemzésünk célja a társadalombiztosítási rendszer keretében közfinanszírozott kardiológiai rehabilitációs fekvőbeteg-ellátás teljesítménymutatóinak feltérképezése Magyarországon. Adatok és módszerek: Elemzésünkhöz a Nemzeti Egészségbiztosítási Alapkezelő (NEAK) finanszírozási adatbázisát használtuk. Az elemzés a 2014 és 2017 közötti időszakot öleli fel. Vizsgáltuk a kardiológiai rehabilitációs ágyak megoszlását, a betegforgalmat, az aktív ellátást követő rehabilitációs arányt. Eredmények: Magyarországon 2017-ben összesen 1765 közfinanszírozott kardiológiai rehabilitációs ágy volt (1,8 ágy/10 000 lakos). A legalacsonyabb ágyszámot Szabolcs-Szatmár-Bereg (0,27 ágy/10 000 lakos), Hajdú-Bihar (0,28) és Fejér (0,6) megyében találtuk. A legmagasabb ágyszámot Veszprém (11,47), Győr-Moson-Sopron (4,94) megyében és Budapesten (2,27) találtuk. Az éves betegszám 2014 és 2017 között 24 834 és 26 146 között, az elszámolt ápolási napok száma 510 ezer és 542 ezer között ingadozott. Az egy betegre jutó átlagos ápolási idő kismértékű emelkedést mutatott, a 2014. évi 19,2 nap/beteg értékről 20,2 nap/beteg értékre nőtt 2017-ben. Az aktív ellátásban akut szívinfarktus miatt hospitalizált betegek 6,6–7,6%-a részesült kardiológiai rehabilitációs fekvőbeteg-ellátásban. Következtetés: Mind a kardiológiai rehabilitációs kapacitásokhoz való hozzáférésben, mind ezen egészségügyi szolgáltatások igénybevételében jelentős területi egyenlőtlenségeket találtunk, melyek mérséklése szakmapolitikai eszközökkel megfontolandó. Az akut szívinfarktuson átesett betegek igen alacsony (6,6–7,6%) részvételi arányát a kardiológiai rehabilitációs ellátásban jelentősen emelni szükséges. Orv Hetil. 2019; 160(Suppl 1): 6–12. | Abstract Introduction: With the improvement of the survival of acute cardiac events and the increasing age, there is a higher demand for cardiac rehabilitation care. Aim: The aim of our study is to analyse the performance indicators of cardiac inpatient rehabilitation care in Hungary financed by the statutory public health insurance system. Data and methods: Data were derived from the financial database of the National Health Insurance Fund of Hungary. We analysed the period between 2014 and 2017. We investigated the distribution of cardiac rehabilitation hospital beds, the patient turnover and the rehabilitation rate following acute care. Results: In 2017, there were 1765 publicly financed cardiac rehabilitation hospital beds in Hungary (1.8 beds/10 000 population). We observed the lowest number of hospital bed number in Szabolcs-Szatmár-Bereg (0.27 beds/10 000 population), Hajdú-Bihar (0.28) and Fejér (0.6) counties. We found the highest number of hospital beds in Veszprém (11.47 beds/10 000 population), Győr-Moson-Sopron (4.94) counties and in Budapest (2.27). Between 2014 and 2017, the annual number of patients was between 24 834 and 26 146, while the number of nursing days varied between 510 thousand and 542 thousand. The average length of stay showed a moderate increase from 19.2 days/patient (2014) to 20.2 days/patient (2017). Only 6.6–7.6% of the patients who underwent acute myocardial infarction received cardiac rehabilitation care. Conclusion: We found significant regional inequalities in both the capacities and the access to and utilization of cardiac rehabilitation healthcare services, which should be mitigated by health policy activities. The low proportion (6.6–7.6%) of patients who underwent acute myocardial infarction and received cardiac rehabilitation care, should be increased. Orv Hetil. 2019; 160(Suppl 1): 6–12

Emergence of Resistant Escherichia coli Mutants in Microfluidic On-Chip Antibiotic Gradients

Spatiotemporal structures and heterogeneities are common in natural habitats, yet their role in the evolution of antibiotic resistance is still to be uncovered. We applied a microfluidic gradient generator device to study the emergence of resistant bacteria in spatial ciprofloxacin gradients. We observed biofilm formation in regions with sub-inhibitory concentrations of antibiotics, which quickly expanded into the high antibiotic regions. In the absence of an explicit structure of the habitat, this multicellular formation led to a spatial structure of the population with local competition and limited migration. Therefore, such structures can function as amplifiers of selection and aid the spread of beneficial mutations. We found that the physical environment itself induces stress-related mutations that later prove beneficial when cells are exposed to antibiotics. This shift in function suggests that exaptation occurs in such experimental scenarios. The above two processes pave the way for the subsequent emergence of highly resistant specific mutations

In situ anaerobic microbiological treatment of a chlorobenzene contaminated groundwater

A one-year site investigation was conducted in a contaminated area near a pharmaceutical industry. The main contaminants were chlorobenzene and benzene. Over time, concentration of the contaminants decreased below regulatory level under anaerobic conditions by biostimulation. To confirm the transformation processes and reveal the mechanisms, a corresponding laboratory microcosm study was set up which completed demonstrating the microbial degradation of these two main pollutants. Assumptions about the transformation processes inferred from field data were confirmed by microcosm studies, consequently necessary supplementary information were provided for bioremediation technologies

Plasticity in Single Axon Glutamatergic Connection to GABAergic Interneurons Regulates Complex Events in the Human Neocortex

In the human neocortex, single excitatory pyramidal cells can elicit very large glutamatergic EPSPs (VLEs) in inhibitory GABAergic interneurons capable of triggering their firing with short (3-5 ms) delay. Similar strong excitatory connections between two individual neurons have not been found in nonhuman cortices, suggesting that these synapses are specific to human interneurons. The VLEs are crucial for generating neocortical complex events, observed as single pyramidal cell spike-evoked discharge of cell assemblies in the frontal and temporal cortices. However, long-term plasticity of the VLE connections and how the plasticity modulates neocortical complex events has not been studied. Using triple and dual whole-cell recordings from synaptically connected human neocortical layers 2-3 neurons, we show that VLEs in fast-spiking GABAergic interneurons exhibit robust activity-induced long-term depression (LTD). The LTD by single pyramidal cell 40 Hz spike bursts is specific to connections with VLEs, requires group I metabotropic glutamate receptors, and has a presynaptic mechanism. The LTD of VLE connections alters suprathreshold activation of interneurons in the complex events suppressing the discharge of fast-spiking GABAergic cells. The VLEs triggering the complex events may contribute to cognitive processes in the human neocortex, and their long-term plasticity can alter the discharging cortical cell assemblies by learning

STRESS INDUCES EQUIVALENT REMODELING OF HIPPOCAMPAL SPINE SYNAPSES IN A SIMULATED POSTPARTUM ENVIRONMENT AND IN A FEMALE RAT MODEL OF MAJOR DEPRESSION

Stress and withdrawal of female reproductive hormones are known risk factors of postpartum depression. Although both of these factors are capable of powerfully modulating neuronal plasticity, there is no direct electron microscopic evidence of hippocampal spine synapse remodeling in postpartum depression. To address this issue, hormonal conditions of pregnancy and postpartum period were simulated in ovariectomized adult female Sprague Dawley rats (n = 76). The number of hippocampal spine synapses and the depressive behavior of rats in an active escape task were investigated in untreated control, hormone-withdrawn 'postpartum', simulated proestrus, and hormone-treated 'postpartum' animals. After 'postpartum' withdrawal of gonadal steroids, inescapable stress caused a loss of hippocampal spine synapses, which was related to poor escape performance in hormone-withdrawn 'postpartum' females. These responses were equivalent with the changes observed in untreated controls that is an established animal model of major depression. Maintaining proestrus levels of ovarian hormones during 'postpartum' stress exposure did not affect synaptic and behavioral responses to inescapable stress in simulated proestrus animals. By contrast, maintaining pregnancy levels of estradiol and progesterone during 'postpartum' stress exposure completely prevented the stress-induced loss of hippocampal spine synapses, which was associated with improved escape performance in hormone-treated 'postpartum' females. This protective effect appears to be mediated by a muted stress response as measured by serum corticosterone concentrations. In line with our emerging 'synaptogenic hypothesis' of depression, the loss of hippocampal spine synapses may be a novel perspective both in the pathomechanism and in the clinical management of postpartum affective illness. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved