Uticaj klimatskih uslova područja na prinos pšenice

The aim of this study was to analyze the influence of climatic conditions in the city of Leskovac, in the period from 2000 to 2008th year, the yield of wheat. This paper presents the average yield of wheat according to the mean monthly temperature and total precipitation during the vegetation period. So they separated two years ago (2003) when he achieved the lowest yield of wheat in the territory of Leskovac (2.4 t ha-1) and the 2004th years ago, when achieved the highest average yield in the period (3.7 t ha- 1). The average yield in the year with favorable schedule and rainfall, and average air temperature was higher by 1.3 t ha-1 of the unfavorable climatic conditions. Deficiency, poor distribution of rainfall, high average temperature, and temperature fluctuations during the growing negative impact on wheat yield. By choosing a variety that is more tolerant to drought, as well as quality and timely application of agro-technical measures can mitigate the adverse impact of climate conditions on the yield of wheat fields.Cilj ovih istraživanja je bio da se analizira uticaj klimatskih uslova na području grada Leskovca, u periodu od 2000.-2008. godine, na prinos pšenice. U radu su prikazani prosečni prinosi pšenice u zavisnosti od srednjih mesečnih temperatura i ukupnih padavina u periodu vegetacije pšenice. Tako su izdvojene dve godine (2003), kada je ostvaren najniži prinos pšenice na teritoriji Leskovca (2.4 t ha-1) i 2004. godina, kada je ostvaren najviši prosečan prinos u posmatranom periodu (3.7 t ha-1). Prosečan prinos u godini sa povoljnijim rasporedom i količinom padavina, kao i srednjom temperaturom vazduha bio je veći za 1.3 t ha-1 od godine sa nepovoljnim klimatskim prilikama. Nedostatak, loš raspored padavina, visoke prosečne temperature, i temperaturna kolebanja u toku vegetacije negativno utiču na prinos pšenice. Izborom sorte koja je tolerantnija prema suši, kao i kvalitetnom i pravovremenom primenom agrotehničkih mera može se ublažiti nepovoljan uticaj klimatskih prilika područja na prinos pšenice

Salicylic Acid Attenuates Gentamicin-Induced Nephrotoxicity in Rats

Gentamicin (GM) is a widely used antibiotic against serious and life-threatening infections, but its usefulness is limited by the development of nephrotoxicity. The present study was designed to determine the protective effect of salicylic acid (SA) in gentamicin-induced nephrotoxicity in rats. Quantitative evaluation of gentamicin-induced structural alterations and degree of functional alterations in the kidneys were performed by histopathological and biochemical analyses in order to determine potential beneficial effects of SA coadministration with gentamicin. Gentamicin was observed to cause a severe nephrotoxicity which was evidenced by an elevation of serum urea and creatinine levels. The significant increases in malondialdehyde (MDA) levels and protein carbonyl groups indicated that GM-induced tissue injury was mediated through oxidative reactions. On the other hand, simultaneous SA administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GM treatment. Exposure to GM caused necrosis of tubular epithelial cells. Necrosis of tubules was found to be prevented by SA pretreatment. The results from our study indicate that SA supplement attenuates oxidative-stress associated renal injury by reducing oxygen free radicals and lipid peroxidation in gentamicin-treated rats

Memory-Like Responses of Brain Microglia Are Controlled by Developmental State and Pathogen Dose

Microglia, the innate immune cells of the central nervous system, feature adaptive immune memory with implications for brain homeostasis and pathologies. However, factors involved in the emergence and regulation of these opposing responses in microglia have not been fully addressed. Recently, we showed that microglia from the newborn brain display features of trained immunity and immune tolerance after repeated contact with pathogens in a dose-dependent manner. Here, we evaluate the impact of developmental stage on adaptive immune responses of brain microglia after repeated challenge with ultra-low (1 fg/ml) and high (100 ng/ml) doses of the endotoxin LPS in vitro. We find that priming of naïve microglia derived from newborn but not mature and aged murine brain with ultra-low LPS significantly increased levels of pro-inflammatory mediators TNF-α, IL-6, IL-1β, MMP-9, and iNOS as well as neurotrophic factors indicating induction of trained immunity (p \u3c 0.05). In contrast, stimulation with high doses of LPS led to a robust downregulation of pro-inflammatory cytokines and iNOS independent of the developmental state, indicating induced immune tolerance. Furthermore, high-dose priming with LPS upregulated anti-inflammatory mediators IL-10, Arg-1, TGF- β, MSR1, and IL-4 in newborn microglia (p \u3c 0.05). Our data indicate pronounced plasticity of the immune response of neonate microglia compared with microglia derived from mature and aged mouse brain. Induced trained immunity after priming with ultra-low LPS doses may be responsible for enhanced neuro-inflammatory susceptibility of immature brain. In contrast, the immunosuppressed phenotype following high-dose LPS priming might be prone to attenuate excessive damage after recurrent systemic inflammation

Small Extracellular Vesicles from Peripheral Blood of Aged Mice Pass the Blood-Brain Barrier and Induce Glial Cell Activation

Extracellular vesicles (EVs), including small EVs (sEVs), are involved in neuroinflammation and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Yet, increased neuroinflammation can also be detected in the aging brain, and it is associated with increased glial activation. Changes in EV concentration are reported in aging tissues and senescence cells, suggesting a role of EVs in the process of aging. Here, we investigated the effect of peripheral sEVs from aged animals on neuroinflammation, specifically on glial activation. sEVs were isolated from the peripheral blood of young (3 months) and aged (24 months) C57BL/6J wildtype mice and injected into the peripheral blood from young animals via vein tail injections. The localization of EVs and the expression of selected genes involved in glial cell activation, including Gfap , Tgf- β , Cd68 , and Iba1 , were assessed in brain tissue 30 min, 4 h, and 24 h after injection. We found that sEVs from peripheral blood of aged mice but not from young mice altered gene expression in the brains of young animals. In particular, the expression of the specific astrocyte marker, Gfap , was significantly increased, indicating a strong response of this glial cell type. Our study shows that sEVs from aged mice can pass the blood-brain barrier (BBB) and induce glial cell activation

A European spectrum of pharmacogenomic biomarkers: Implications for clinical pharmacogenomics

Pharmacogenomics aims to correlate inter-individual differences of drug efficacy and/or toxicity with the underlying genetic composition, particularly in genes encoding for protein factors and enzymes involved in drug metabolism and transport. In several European populations, particularly in countries with lower income, information related to the prevalence of pharmacogenomic biomarkers is incomplete or lacking. Here, we have implemented the microattribution approach to assess the pharmacogenomic biomarkers allelic spectrum in 18 European populations, mostly from developing European countries, by analyzing 1,931 pharmacogenomics biomarkers in 231 genes. Our data show significant interpopulation pharmacogenomic biomarker allele frequency differences, particularly in 7 clinically actionable pharmacogenomic biomarkers in 7 European populations, affecting drug efficacy and/or toxicity of 51 medication treatment modalities. These data also reflect on the differences observed in the prevalence of high-risk genotypes in these populations, as far as common markers in the CYP2C9, CYP2C19, CYP3A5, VKORC1, SLCO1B1 and TPMT pharmacogenes are concerned. Also, our data demonstrate notable differences in predicted genotype-based warfarin dosing among these populations. Our findings can be exploited not only to develop guidelines for medical prioritization, but most importantly to facilitate integration of pharmacogenomics and to support pre-emptive pharmacogenomic testing. This may subsequently contribute towards significant cost-savings in the overall healthcare expenditure in the participating countries, where pharmacogenomics implementation proves to be cost-effective

TOPOGRAPHIC IDENTIFICATION OF THE PONTOMEDULLARY RESPIRATORI-SENSITIVE NUCLEI OF THE RAT BRAIN BY GLUTAMATE MICRO-STIMULATIONS

Automatic control of breathing is highly dependent on the integrity of the pontomedullary network of reciprocally connected neurons localized in a number of functionally and neurochemically different compartments. Glutamate is considered the key neurotransmitter mediating signal transmission in the respiratory regions of the brainstem. Identification of the respiratory-sensitive neurons using this neurotransmitter for microstimulations provides an insight into the topographic organization of the pontomedullary nuclei involved in the modulation and control of breathing.Three types of respiratory responses were observed following glutamate microinjections: hyperpnea, apneusis (inspiratory cramp) and hypopnea or apnea. Hyperpnea was obtained as a result of microstimulations in the region of lateral parabrachium and caudal Kölliker-Fuse nuclei. Apneustic response was observed in the region localized ventrally from superior cerebellar peduncle, while hypopneic or apneic responses followed glutamate microinjections in the region of ventral Kölliker-Fuse nucleus and a narrow area between motor and principal sensory trigeminal nucleus, which is referred to as intertrigeminal region.Anatomical distribution of the obtained respiratory responses depends on the localization of microinjections and ascendant and descendent projections stemming from the sites of stimulation

Lycopene improves methotrexate-induced functional alterations of the Madin-Darby kidney cells in a concentration-dependent manner

Lycopene is one of the most potent antioxidants among carotenoids due to its ability to quench singlet oxygen and react with free radicals to reduce DNA damage. Methotrexate is widely used in the treatment of several types of cancers and autoimmune diseases. One of the most common side effects of high-dose of methotrexate is kidney injury. In this study we evaluated effects of lycopene on the Madin-Darby canine kidney cells (MDCK)treated with methotrexate through the estimation of their mitochondrial and lysosomal functions (MTT reduction assay and NR uptake assay) and changes in cell oxidative status (determination of advanced oxidized proteins concentrations and reduced glutathione levels) and lysosomal enzymes activity (β-N acetyl glucosaminidase activity).Results of our study showed that lycopene applied in high concentration caused significant impairment of the MDCK function leading to cell death. Contrary, in relatively low concentrations lycopene moderately ameliorated methotrexate-induced MDCK cells’ death estimated by both biochemical and microscopic analyses. It also prevented a significant decline in the MDCK cells’ lysosomal function estimated by neutral red accumulation ability and activity of lysosomal enzyme β-N acetyl glucosaminidase.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Low intensity exercise in the prevention of cardiac insulin resistance-related inflammation and disturbances in NOS and MMP-9 regulation in fructose-fed ovariectomised rats

Exercise is important nonpharmacological treatment for improvement of insulin sensitivity in menopause. However, its effect on menopausal cardiac insulin resistance is needing further research. We investigated protective effects of low intensity exercise on cardiac insulin signaling, inflammation, regulation of nitric oxide synthase (NOS) and matrix metalloproteinase 9 (MMP-9) in ovariectomised (OVX) Wistar rats, submitted to 10% fructose solution during 9 weeks. OVX rats were divided into control, sedentary fructose and exercise fructose group. Measurements of physical and biochemical characteristics were carried out to evaluate metabolic syndrome development. mRNA and protein levels and phosphorylation of cardiac insulin signaling molecules, endothelial and inducible NOS (eNOS and iNOS), p65 subunit of nuclear factor κB (NFκB), tumor necrosis factor α (TNF-α), suppressor of cytokine signalling 3 (SOCS3) and MMP-9 were analysed. Fructose increased insulin level, HOMA index and visceral adipose tissue weight, while low intensity exercise prevented insulin level and HOMA index increase. Fructose also decreased cardiac pAkt (Ser473), peNOS (Ser1177) and increased insulin receptor substrate 1 (IRS1) phosphorylation at Ser307, pNFκB (Ser276) and NFκB and MMP-9 content, without effects on iNOS, protein-tyrosine phosphatase 1B, TNF-α and SOCS3. Exercise prevented changes in pIRS1 (Ser307), pAkt (Ser473), peNOS (Ser1177), pNFκB (Ser276) and NFκB expression. In addition, exercise increased pIRS1 (Tyr632), pAkt (Thr308) and eNOS expression. The low intensity exercise prevented cardiac insulin signaling disarrangement in fructose-fed OVX rats and therefore eNOS dysfunction, as well as pro-inflammatory signaling activation, without effect on tissue remodeling, suggesting physical training as a tool for reduction of cardiovascular risk.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author