Authors:Anna Blázovics, Péter Sipos, Ibolya Kocsis, Hedvig Fébel, Dénes Kleiner, Klára Szentmihályi and Erzsébet Fehér
Bevezetés: A zsírmáj kialakulhat betegségek, műtétek,
gyógyszerek, éhezés vagy túlzott mértékű alkoholfogyasztás következtében, de a
helytelen táplálkozást, a zsírbő és rostszegény étkezést tartják az elsődleges
oknak. A nem alkoholos zsírmájbetegség a lakosság 20–30%-át érintheti. A
táplálkozási eredetű zsírmájat korai stádiumban általában szövődménymentes
májkárosodásnak írják le. Célkitűzés: Kutatásaink célja a
zsírdús táplálkozás bél–máj tengelyre gyakorolt hatásának a feltérképezése volt.
Módszerek: Rutinlaboratóriumi, analitikai és szövettani
módszerekkel patkányokban vizsgáltuk a bél és a máj redoxparamétereit, valamint
a máj zsírsavösszetételét és elemtartalmát. Eredmények: A máj
elzsírosodása során a vérszérumban mérhető májenzim- és metabolitértékek
eltérései mellett a redox-homeosztázis mutatóiban is szignifikáns változások
igazolódtak. Változás volt kimutatható a májban, a vérben és a belekben. A máj
elzsírosodásának folyamata együtt jár a transzmetiláló képesség csökkenésével.
Megváltozott a zsírsavösszetétel és a fémion-homeosztázis is a májban.
Szövettani vizsgálatoknál a májlobulusok centrális részén a hepatocyták
megduzzadtak, bennük zsírcseppek láthatók, piknotikus sejtmagok alakultak ki,
ami a zsíros elfajulásra jellemző. A vékony- és vastagbél enterocytái sérültek,
helyenként lelökődtek a felszínről, és gyulladásos reakciók figyelhetők meg a
nyálkahártyában. Következtetés: Eredményeink alapján
leszögezhető, hogy a zsírdús diéta okozta steatosis már korai stádiumban sem
tekinthető egyszerűen reverzibilis változásnak, mert a változások kedvezőtlenül
befolyásolják az egész szervezet redox-homeosztázisát, és egyben alapját
képezhetik súlyos szív- és metabolikus betegségeknek, valamint siettethetik a
gastrointestinalis tumorok kialakulását. Orv Hetil. 2020; 161(35):
Authors:A. Lelbach, G. Dörnyei, F. Ihász and A. Koller
By now, there is no doubt that regular physical exercise has an overall beneficial effect on each organ of the body. However, the effects of highly competitive sports (HCS) are more complex, as they exert greater demands on the cardiovascular and metabolic systems, among others. Strength, athletic, and aesthetic sport types each has a different exercise intensity and nutritional loading, as well as a different prevalence of cardiometabolic diseases at a later age. HCS athletes experience hypertension and mental stress during competitions and high nutritional loads between them. The post-career effects of this behaviour on the heart, arteries, cellular metabolism, and risk of obesity, are not well known and are not often the focus of research. In this review, we aimed to summarize the post-career effects of HCS. Based on data in the literature, we propose that athletes involved in highly competitive strength sports progressively develop metabolic syndrome and sustained elevated blood pressure.
Authors:J. Chen, L. Wang, W.H. Liu, J. Shi, Y. Zhong, S.J. Liu and S.M. Liu
Although the use of aspirin has substantially reduced the risks of cardiovascular events and death, its potential mechanisms have not been fully elucidated. In a previous study, we found that aspirin triggers cellular autophagy. In the present study, we aimed to determine the protective effects of aspirin on human coronary artery endothelial cells (HCAECs) and explore its underlying mechanisms. HCAECs were treated with oxidized low-density lipoprotein (ox-LDL), angiotensin II (Ang-II), or high glucose (HG) with or without aspirin stimulation. The expression levels of endothelial nitric oxide (NO) synthase (eNOS), p-eNOS, LC3, p62, phosphor-nuclear factor kappa B (p-NF-κB), p-p38 mitogen-activated protein kinase (p-p38 MAPK), and Beclin-1 were detected via immunoblotting analysis. Concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured via ELISA. NO levels were determined using the Griess reagent. Autophagic flux was tracked by tandem mRFP-GFP-tagged LC3. Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner. Aspirin also increased the LC3II/LC3I ratio, decreased p62 expression, and enhanced autophagic flux (autophagosome and autolysosome puncta) in the HCAECs. p-NF-κB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1. These results suggested that aspirin can protect ECs from ox-LDL-, Ang-II-, and HG-induced injury by activating autophagy in a Beclin-1-dependent manner.
Authors:Sara Asadi, Parvin Farzanegi and Mohammad Ali Azarbayjani
Knee osteoarthritis (OA) is a common type of degenerative joint disease which decreases the quality of life. Sex-determining region Y box 9 (SOX9) and hypoxia-inducible factor-1 (HIF1) are considered as the key regulators of OA. We investigated the effect of combined therapies with mesenchymal stem cells (MSCs), ozone (O3) and exercise training on SOX9 and HIF1 expression in the cartilage of rats with knee OA.
Knee OA was induced by surgical method. OA rats were divided into model, MSCs, ozone, exercise, MSCs + ozone, MSCs + exercise, ozone + exercise and MSCs + ozone + exercise groups. Rats in the MSCs group received intraarticular injection of 1 × 106 cells/kg. Rats in the ozone group received O3 at the concentration of 20 μg/mL, once weekly for 3 weeks. Rats in the exercise group were trained on rodent treadmill three times per week. 48 hours after the programs, cartilage tissues were isolated and the expression of SOX9 and HIF1 was determined using Real-Time PCR.
Significant differences were found in the expression of SOX9 and HIF1 between groups (P < 0.0001). Although combined therapies with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 in the cartilage tissue of rats with knee OA, combination of exercise with O3 was significantly more effective compared to the other combined therapies (P < 0.001).
Combined therapy with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 genes in the cartilage of rats with knee OA; however, exercise + O3 was significantly more effective.
Authors:F.S. Sajjadi, F. Aghighi, Z. Vahidinia, A. Azami-Tameh, M. Salami and S.A. Talaei
Exposure to noise stress during early life may permanently affect the structure and function of the central nervous system. The aim of this study was to evaluate the effects of prenatal exposure to urban traffic noise on the spatial learning and memory of the rats' offspring and the expression of glucocorticoid receptors (GRs) in their hippocampi.
Three g\roups of pregnant rats were exposed to recorded urban traffic noise for 1, 2 or 4 h/day during the last week of pregnancy. At the age of 45 days, their male offspring were introduced to the Morris water maze (MWM) for assessment of spatial learning and memory. The corticosterone levels were measured in the offspring's sera by radioimmunoassay, and the relative expression of glucocorticoid and mineralocorticoid receptors (MRs) in their hippocampi was evaluated via RT-PCR.
Facing urban traffic noise for 2 and 4 h/day during the third trimester of pregnancy caused the offspring to spend more time and to travel a larger distance than the controls to find the target platform. Analogously, these two groups were inferior to their control counterparts in the probe test. Also, prenatal noise stress elevated the corticosterone concentration in the sera of the rats' offspring and dose-dependently decreased the relative expression of the mRNA of both GRs and MRs in their hippocampi.
Urban traffic noise exposure during the last trimester of pregnancy impairs spatial learning and memory of rat offspring and reduces GRs and MRs gene expression in the hippocampus.
A considerable number of patients arriving in dental offices are being treated with ongoing medication for a variety of chronic diseases. As a result, dentists must be familiar with the potential side effects these therapeutic agents may have on the tissues of the oral cavity, and in particular on the salivary gland. Salivary gland function may be altered by a wide range of medications, leading to effects such as xerostomia, hyposalivation, hypersalivation or even swelling of the glands. These disorders can cause a variety of other health complications. This review will focus on the most common groups of drugs responsible for salivary gland dysfunction, including psychoactive drugs, antidepressants, antipsychotics, antihypertensives, and antihistamines.
Authors:E. Kovács, D. Pilecky, Z. Szakál-Tóth, A. Fekete-Győr, V.A. Gyarmathy, L. Gellér, B. Hauser, J. Gál, B. Merkely and E. Zima
We investigated the effect of age on post-cardiac arrest treatment outcomes in an elderly population, based on a local database and a systemic review of the literature.
Data were collected retrospectively from medical charts and reports. Sixty-one comatose patients, cooled to 32–34 °C for 24 h, were categorized into three groups: younger group (≤65 years), older group (66–75 years), and very old group (>75 years). Circumstances of cardiopulmonary resuscitation (CPR), patients' characteristics, post-resuscitation treatment, hemodynamic monitoring, neurologic outcome and survival were compared across age groups. Kruskal-Wallis test, Chi-square test and binary logistic regression (BLR) were applied. In addition, a literature search of PubMed/Medline database was performed to provide a background.
Age was significantly associated with having a cardiac arrest on a monitor and a history of hypertension. No association was found between age and survival or neurologic outcome. Age did not affect hemodynamic parameter changes during target temperature management (TTM), except mean arterial pressure (MAP). Need of catecholamine administration was the highest among very old patients. During the literature review, seven papers were identified. Most studies had a retrospective design and investigated interventions and outcome, but lacked unified age categorization. All studies reported worse survival in the elderly, although old survivors showed a favorable neurologic outcome in most of the cases.
There is no evidence to support the limitation of post-cardiac arrest therapy in the aging population. Furthermore, additional prospective studies are needed to investigate the characteristics and outcome of post-cardiac arrest therapy in this patient group.
Authors:N. Hoeller, N. Baik-Schneditz, B. Schwaberger, L. Mileder, B. Urlesberger and G. Pichler
To investigate the ratio of cerebral tissue oxygenation index (cTOI) to peripheral muscle tissue oxygenation index (pTOI) measured by near-infrared spectroscopy (NIRS) in cardio-circulatory stable preterm neonates without signs of inflammation/infection on the first day after birth.
Observational study analysing secondary outcome parameters of the ‘Avoiding Hypotension in Preterm Neonates (AHIP)’ trial (ClinicalTrials.gov identifier: NCT01910467). Preterm neonates, who had cTOI and pTOI measurements during 24 h after birth, were included. In each neonate the mean of the cTOI/pTOI-ratio, cTOI, pTOI and routine monitoring parameters were calculated for each hour and for the 24-h measuring period. Courses of all measured parameters were analysed.
Eighty-seven stable preterm neonates (33.1 [32.1–34.1] weeks of gestation) were included. The mean value over the 24-h measuring period for the cTOI/pTOI-ratio was 0.96 ± 0.02, for cTOI 70.1 ± 1.4 and for pTOI 73.4 ± 0.9. Routine monitoring parameters were in the normal ranges over 24 h. The courses of the cTOI/pTOI-ratio and cTOI showed significantly lower values from hour 5 to 15 compared to the first hours after birth. Heart rate decreased significantly over time, whereas mean arterial blood pressure increased significantly. pTOI, arterial oxygen saturation and body temperature showed no significant change over time.
We are the first to report on cTOI/pTOI-ratios for cardio-circulatory stable preterm neonates over a 24-h period after birth, showing significantly lower values from hour 5 to 15 compared to the first hours after birth.
Authors:Zs. Sári, T. Kovács, T. Csonka, M. Török, É. Sebő, J. Toth, D. Tóth, E. Mikó, B. Kiss, D. Szeőcs, K. Uray, Zs. Karányi, I. Kovács, G. Méhes, P. Árkosy and P. Bai
Breast cancer is characterized by oncobiosis, the abnormal composition of the microbiome in neoplastic diseases. The biosynthetic capacity of the oncobiotic flora in breast cancer is suppressed, as suggested by metagenomic studies. The microbiome synthesizes a set of cytostatic and antimetastatic metabolites that are downregulated in breast cancer, including cadaverine, a microbiome metabolite with cytostatic properties. We set out to assess how the protein expression of constitutive lysine decarboxylase (LdcC), a key enzyme for cadaverine production, changes in the feces of human breast cancer patients (n = 35). We found that the fecal expression of Escherichia coli LdcC is downregulated in lobular cases as compared to invasive carcinoma of no special type (NST) cases. Lobular breast carcinoma is characterized by low or absent expression of E-cadherin. Fecal E. coli LdcC protein expression is downregulated in E-cadherin negative breast cancer cases as compared to positive ones. Receiver operating characteristic (ROC) analysis of LdcC expression in lobular and NST cases revealed that fecal E. coli LdcC protein expression might have predictive values. These data suggest that the oncobiotic transformation of the microbiome indeed leads to the downregulation of the production of cytostatic and antimetastatic metabolites. In E-cadherin negative lobular carcinoma that has a higher potential for metastasis formation, the protein levels of enzymes producing antimetastatic metabolites are downregulated. This finding represents a new route that renders lobular cases permissive for metastasis formation. Furthermore, our findings underline the role of oncobiosis in regulating metastasis formation in breast cancer.