Number of analyzed days in specified data groups according to F10.7 range and month. The last column shows mean number of days per F10.7 range.
\r\n\t
\r\n\tThe aim of this book project is to compile the updated research work on medicinal applications of noble metal complexes mainly focusing the structure activity relationship of metal complexes with targeting biological components.
Nowadays, the Global Navigation Satellite System (GNSS) is commonly used for positioning, navigation and timing. The GNSS based services are used in many areas such as maritime, aviation, agriculture, public transportation and geodesy. The GNSS receiver computes its position by trilateration using ranges between satellites and the receiver, where the ranges are calculated from measurements of time-of-arrival of satellite radio signals [1]. However, the signals do not propagate ideally. Many factors can change signals’ propagation speed or trajectory and they can consequently cause incorrect determination of the receiver position.
One of the factors which affect GNSS signal propagation is the ionosphere. The ionosphere causes delay of radio signals, and if not mitigated, it can be the largest source of error (ionospheric error) in GNSS positioning and navigation [2]. There are several possibilities to compensate for the ionospheric effect. First technique is to use multi-frequency satellite-receiver communication which takes advantages of dispersive nature of the ionosphere. This approach called ionosphere-free combination can remove about 99 % of the ionospheric error [3]. In case the receiver uses only one frequency it can use a Satellite Based Augmentation Systems (SBAS) such as the Wide Area Augmentation System (WAAS) or European Geostationary Navigation Overlay Service (EGNOS). These systems determine condition of nearby ionosphere from a network of reference stations and send the information to the user via a geostationary satellite [4]. If the SBAS service is not available or it is not supported by the receiver, an ionospheric model can be used to estimate the ionospheric error. Ionospheric models are also used for satellite and receiver inter-frequency bias estimation and Total Electron Content (TEC) calibration [5].
There are several empirical ionospheric models. Well known empirical models included in our study are the Klobuchar model, International Reference Ionosphere (IRI) and NeQuick. In addition, we evaluated accuracy of a relatively new model developed at DLR (Deutsches Zentrum für Luft-und Raumfahrt), the Neustrelitz TEC Model (NTCM) [6]. As each of the models applies different modeling approach and was developed with different background data, we assume that their TEC modeling performance differ and the use of one model in particular condition would be better than use of another.
Some of the recent analysis evaluated TEC modeling performance of the Klobuchar model and the NeQuick 2 by comparison of modeled TEC with GNSS measurements [7], [8]. In our study, we evaluated performance of four empirical ionospheric models comparing them with Global Ionospheric Maps (GIMs) produced at the Center for Orbit Determination in Europe (CODE), using a similar approach as in [9] for the Klobuchar model and the NeQuick 2. This approach has the advantage that all TEC data are in the zenith direction, therefore, we can avoid conversion between slant and vertical TEC which can produce additional error [10]. On the other hand, GIMs do not contain direct measurements and we have to consider their data accuracy.
To estimate TEC mismodeling for each model, we compared modeled TEC data with CODE GIMs over three years (2010, 2011 and 2012). Such data were produced at the CODE using measurements from about 200 GPS/GLONASS stations. The evaluation will show variation in models\' TEC modeling performance with respect to time of day, season, location and space weather condition. In addition, it will show in which cases the CODE GIMs\' inaccuracy prevents performance evaluation.
The ionosphere is the part of the atmosphere with large amount of charged particles (ions and electrons). A typical vertical profile of ionospheric electron density (Figure 1) is divided into the several layers according to the different ionization and recombination principles [11]. The ionospheric structure significantly varies with geographical location, local time and with changes in solar-terrestrial environment.
We can divide ionospheric variations into two groups. The first group includes variations with periodic behavior that can be distinguished from empirical data. These variations are: daily variation, seasonal variation, dependence on the geomagnetic field and climatological dependence on space weather. These phenomena can be analytically described and modeled by empirical ionospheric models.
The second group of ionospheric variations includes sudden ionospheric disturbances (SID) or small rapid changes in the electron density causing scintillation. Even though these phenomena are often observed, they do not show any behavior pattern to the magnitude or period of occurrence [12]. As these variations belong to ionospheric weather rather than to climatology they are not modeled by empirical ionospheric models.
A typical vertical electron density profile of the ionosphere. The electron density profile during day and night is represented by full and dashed line, respectively. The dotted line shows the average height of the daily electron density maximum. The picture was made by the authors according to [13].
Radio signal which propagates through the ionosphere experiences changes of its propagation speed and trajectory. These changes depend on the signal carrier frequency and electron density of the ionosphere [14]. The ratio between the group propagation velocity
The refractive index of the ionosphere
where
The integration of the electron density along the path is usually referred to as Total Electron Content (TEC):
which is the total number of electrons in a tube of 1 m2 cross-section along the GNSS signal path through the ionosphere. If we know the frequency of the signal, the value of TEC allows us to compute the propagation delay introduced by the ionosphere, which is an error for our point of view. All ionospheric models considered in this study can provide TEC values.
There are two commonly used types of TEC values: vertical and slant TEC. Vertical total electron content (vTEC) at a certain geographical point stands for TEC in the direction of the zenith. TEC between a satellite and a receiver is usually referred to as the slant TEC (sTEC). This notation signifies that the TEC is at a different angle then the zenith. TEC is usually given in TEC Units (TECU) where 1 TECU=1016 electrons/m2.
The Klobuchar model was developed by John A. Klobuchar at the Air Force Geophysics Laboratory, U.S. The algorithm is used to correct ionospheric time-delay in GPS for single frequency communication. The model was developed in 1975 keeping in mind limited computation memory and capability of receivers, therefore, the model algorithm is very fast and has minimum complexity.
One of the main criteria of the algorithm design was to fit best the daily period with the largest TEC values, i.e. afternoon period. The Klobuchar model approximates daytime variation of ionospheric time delay as a half period of cosine function with maximum at 14 hours local time. The amplitude and period of the cosine are each calculated with 4 coefficients transmitted by GPS navigation message. The night time ionospheric delay is set as a constant value of 5 ns (Figure 2.) [16].
Global ionospheric map of 26th February 2010, 12 UT modeled by the Klobuchar model.
The first version of the International Reference Ionosphere was developed as a joint project of Committee on Space Research (COSPAR) and Union of Radio Science (URSI) in 1978. Since then, the model has been continuously improving.
The IRI is able to compute vertical electron density profile and vTEC as well as other ionospheric parameters such as ion densities and ion temperatures. The IRI divides the ionosphere into six sub-regions where each of them is described by several parameters. The model also uses lists of foF2 and M(3000)F2 parameters (foF2 is critical frequency of the ionospheric layer F2 which is usually the layer with Ne maximum, M(3000)F2 is ratio between maximum usable frequency for ionospheric radio link over the distance of 3000 km using layer F2 and foF2, more information can be found in [17]). The integration height for TEC computation is limited to 2000 km [18].
To calculate vertical el. density profile of the ionosphere, user can choose one from several models for each region. In this work, we used standard IRI setting. The IRI uses both space weather and geomagnetic indices, i.e. Solar Radio Flux (F10.7) index, International Sunspot Number (Ri) and magnetospheric Ap index which describes variations in the Earth\'s geomagnetic field.
Comparing to the Klobuchar model, the ionosphere structure modeled by the IRI is more complex including also the equatorial anomaly (Figure 3). Equatorial anomaly is the area with higher TEC distanced about 20° north and south from the equator. Source code of current IRI version is available on model\'s webpage (http://irimodel.org/).
Global ionospheric map of 26th February 2010, 12 UT modeled by the IRI2012.
The NeQuick is an empirical model based on the model introduced by Di Giovanni and Radicella in 1990. Its modified version is used in the GNSS Galileo to aid single-frequency positioning [19]. The model has been also included into the ITU-R recommendation as a suitable method for TEC modeling. In addition, the IRI model uses NeQuick algorithm as a default option for the upper ionosphere computation.
The NeQuick is able to calculate electron density at any given location in the ionosphere. Therefore, it can provide TEC and electron density profile between any two given points [20]. For the analyses, we used the NeQuick version 2 which we obtain at the International Centre for Theoretical Physics in Trieste, Italy. The model is driven by monthly-mean solar radio flux.
NeQuick is a complex electron density model. As well as in case of the IRI, we can distinguish equatorial anomaly on the NeQuick GIM (Figure 4).
Global ionospheric map of 26th February 2010, 12 UT modeled by the NeQuick 2 model.
Recently, a new global ionospheric model NTCM was developed at the Institute of Communications and Navigation, DLR in Neustrelitz, Germany. The model can provide values of vTEC at any given time and location. The core of the model consists of 12 coefficients which can be autonomously used for full solar cycle. The driver of the NTCM is the F10.7 index. The model does not use any integration of electron density profile, therefore, it is very simple and fast [5]. The model analytically describes daily variation, seasonal variation, equatorial altitude anomaly and solar flux dependency as harmonic functions. All the formulas of the model algorithm can be found in [6].
The NTCM, as well as the Klobuchar, is a TEC model. The GIM structure is rather simple and more similar to the Klobuchar one than to the GIMs produces with the electron density models IRI and NeQuick (Figure 5).
Global ionospheric map of 26th February 2010, 12 UT modeled by the NCTM model.
All the ionospheric models discussed here are climatological. For our comparison, we chose CODE as a form of climatological reference rather than real measurements which can be affected by local ionosphere weather.
The Center for Orbit Determination in Europe at the Astronomical Institute at University of Berne, Switzerland provides GIMs on daily bases from 1995. The maps are available in the IONosphere map EX change format (IONEX) from 1997. CODE GIMs cover area from 87.5° northern to 87.5° southern latitude and from 180° western to 180° eastern longitude. The grid point step is 2.5° in latitude and 5° in longitude. GIMs are produced with 2 hours interval and the maps are generated using data from about 200 GPS/GLONASS sites of the IGS (International GNSS Service) and other institutions. Each map grid point contains a vTEC value calculated from measurements from the GNSS sites [21].
The accuracy of the CODE vTEC values depends on the local density of the GNSS reference network. The reference stations are not equally distributed over the whole world and CODE has higher level of inaccuracy at places with lack of reference stations, typically over oceans. Along vTEC values, CODE IONEX files contain also RMS maps (Figure 6) which give value of RMS error for each GIM grid point.
Averaged map of all the RMS error values of CODE maps during years 2010, 2011, and 2012.
As the goal is a climatological study a lot of data are required. In this study, we processed data from years 2010, 2011, and 2012. Considering 12 maps per day and 2012 as a leap year, we made comparisons with 13,152 CODE maps. As each map has 71x73 (±87.5 latitude with 2.5° step, ±180 longitude with 5° step) values, we processed 68,166,816 CODE values in total.
First, we created similar GIM databases as the CODE one with all 4 models so that, for each CODE map, we created 1 map for each ionospheric model (4 maps per 1 CODE map). The modeled maps have the same grid points as CODE maps and each grid point contains corresponding modeled vTEC value.
As the next step, we divided data into groups. First division was according to the universal time (UT). For example, maps for 12 UT were compared only with each other and not with maps for different UT. As the CODE time resolution is 2 hours, this division created 12 data groups. Secondly, we divided data according to months in order to analyze effect of seasonal variation. This division created 12 month sub-groups for each of the 12 UT data groups.
The last division criterion was solar activity. Solar radio flux F10.7 and international sunspot number Ri are considered to be two primary long-term solar indices. The F10.7 is often used as a proxy for Ri making these two indices interchangeable, however, a recent study showed that there is a disagreement during the last decade [22]. We chose F10.7 over the Ri as we assume that the index derived from measurements on Earth surface corresponds more to the ionospheric behavior rather than index derived from measurements of a solar phenomena (sun spots). The Figure 7 shows the observed solar radio flux variation for years 2010, 2011, and 2012. The data for the 1st of January 2011 and 2012 were missing and were filled as linear interpolation of values of adjacent days.
Considering 3 years of data, each group has approximately 91 days (e.g. March group has 93 days as 3 years mean 3 Marches (3x31=93)). To keep the number of days within one F10.7 group high enough we decided to divide the groups into only 4 F10.7 sub-groups. Applying this division, each sub-group should have approximately 23 days where every sub-group includes only days within particular F10.7 range. We divided the dataset in order to keep the amount of days in groups as balances as possible, which led to non uniform distribution of F10.7 intervals (Figure 7). Even so, some groups have significantly less or more days then ideal 23 days (Table 1).
Variation of observed F10.7 for years 2010, 2011, and 2012. The green lines divide the F10.7 into ranges.
\n\t\t\t\tF10.7 range [sfu]\n\t\t\t | \n\t\t\t\n\t\t\t\tNumber of days per group\n\t\t\t | \n\t\t\t\n\t\t\t\tmean\n\t\t\t | \n\t\t|||||||||||
\n\t\t\t | \n\t\t\t | \n\t\t\t | \n\t\t\t | \n\t\t\t | \n\t\t\t\tMonth\n\t\t\t | \n\t\t\t\n\t\t\t | \n\t\t\t | \n\t\t | |||||
1. | \n\t\t\t2. | \n\t\t\t3. | \n\t\t\t4. | \n\t\t\t5. | \n\t\t\t6. | \n\t\t\t7. | \n\t\t\t8. | \n\t\t\t9. | \n\t\t\t10. | \n\t\t\t11. | \n\t\t\t12. | \n\t\t||
0 – 82 | \n\t\t\t32 | \n\t\t\t13 | \n\t\t\t11 | \n\t\t\t30 | \n\t\t\t32 | \n\t\t\t30 | \n\t\t\t19 | \n\t\t\t20 | \n\t\t\t14 | \n\t\t\t13 | \n\t\t\t13 | \n\t\t\t12 | \n\t\t\t19.9 | \n\t\t
83 – 100 | \n\t\t\t30 | \n\t\t\t37 | \n\t\t\t28 | \n\t\t\t9 | \n\t\t\t17 | \n\t\t\t27 | \n\t\t\t40 | \n\t\t\t30 | \n\t\t\t19 | \n\t\t\t20 | \n\t\t\t23 | \n\t\t\t25 | \n\t\t\t25.4 | \n\t\t
101 – 122 | \n\t\t\t6 | \n\t\t\t34 | \n\t\t\t38 | \n\t\t\t43 | \n\t\t\t30 | \n\t\t\t15 | \n\t\t\t12 | \n\t\t\t30 | \n\t\t\t20 | \n\t\t\t17 | \n\t\t\t10 | \n\t\t\t26 | \n\t\t\t23.4 | \n\t\t
> 122 | \n\t25 | \n\t1 | \n\t18 | \n\t8 | \n\t14 | \n\t18 | \n\t22 | \n\t13 | \n\t37 | \n\t43 | \n\t44 | \n\t30 | \n\t22.8 | \n
Number of analyzed days in specified data groups according to F10.7 range and month. The last column shows mean number of days per F10.7 range.
We estimated the TEC mismodeling of all models comparing the modeled ionospheric maps with the reference CODE maps for each data group. We calculated the mismodeling as mean absolute difference between model\'s and CODE\'s
where
As it was mentioned, the accuracy of CODE data varies and should be considered. We calculated mean CODE RMS error
where the N is again the number of analyzed maps for each data group.
The decision of the most accurate model was made for each map grid point of each data group. Referring to Figure 8, in case the
Block scheme of decision making of the best model for one grid point.
Results for each field of Table 1 are represented in form of grid maps. As there are 48 groups and each of them has 12 UT-sub-groups we do not show all the results but only two examples. It should be noted that all the shown maps display interpolated data (1° x 1°) but the original grid resolution is 2.5° in latitude and 5° in longitude.
The first example (Figure 9) shows results for October, 14 UT and F10.7 range of 101 – 122 sfu. Figure 9a shows
Global maps for October, 14 UT and F10.7 range of 101 – 122 sfu. The top left map shows values of mean difference between the TEC values of selected best models and CODE TEC (a). The top right map shows the best models distribution over the globe (b). The third map shows mean RMS error of CODE data for this data group (c) and on four map we marked regions for which it is not possible to decide of the most accurate (gray-white stripes, d). The last map shows the areas where two models have TECdiff lower then CODE RMS error (e).
The second example of results is for January, 02 UT for 0 – 82 sfu data group (Figure 10). As it was expected, the
Global maps for January, 02 UT and F10.7 range of 0 – 82 sfu. The top left map shows values of mean difference between the TEC values of selected best models and CODE TEC (a). The top right map shows the best models distribution over the globe (b). At the third map we marked the regions for which it is not possible to decide of the best model (gray-white stripes, c). The last map shows the areas where two of four models have TECdiff lower then CODE RMS values (d).
The results can be also expressed in form of a graph for particular location. Both Figure 11 and 12 show performance of the models for the location: 60° northern latitude and 15° eastern longitude. Results for October, 14 UT and 101 – 122 sfu is shown in Figures 11 and results for January, 02 UT and 0 – 82 sfu in Figure 12. The graph for October shows that in all cases there is no more than one model with
Variation of the mean difference between model and CODE TEC values for October 14 UT and F10.7 range of 101 – 122 sfu. The black dashed line signifies the mean CODE RMS error.
Variation of the mean difference between model and CODE TEC values for January, 02 UT and F10.7 range of 0 – 82 sfu. The black dashed line signifies the CODE RMS error value.
If we summarize results for all data groups we can show how much were models identified as the best with respect to different areas (Table 2). The EU region was chosen between 65° – 30° northern latitude and 10° western to 50° eastern longitude and the USA between 55° – 0° northern latitude and 130° – 50° western longitude. Similar results but with respect to F10.7 ranges are shown in Table 3. Table 4 summarizes the amount of cases for which the analysis was able to decisively determine the best model with respect to both F10.7 and different regions.
\n\t\t\tModel\n\t\t | \n\t\t\n\t\t\tPortion cases [%]\n\t\t | \n\t||
\n\t\t | \n\t\t\tRegion\n\t\t | \n\t||
\n\t\t\tAll data [%]\n\t\t | \n\t\t\n\t\t\tDecisive EU [%]\n\t\t | \n\t\t\n\t\t\tDecisive USA [%]\n\t\t | \n\t|
IRI2012 | \n\t\t19.1 | \n\t\t14.9 | \n\t\t16.3 | \n\t
Klobuchar | \n\t\t32.9 | \n\t\t44.0 | \n\t\t41.1 | \n\t
NeQuick2 | \n\t\t18.9 | \n\t\t13.7 | \n\t\t11.9 | \n\t
NTCM | \n\t\t29.1 | \n\t\t27.4 | \n\t\t30.7 | \n\t
Amount of cases the models were decisively identified as the best one for different regions considering all data.
\n\t\t\tRegion\n\t\t | \n\t\t\n\t\t\tPortion of cases [%]\n\t\t | \n\t|||
\n\t\t | \n\t\t\tF10.7 range [sfu]\n\t\t | \n\t|||
0 – 82 | \n\t\t83 – 100 | \n\t\t101 – 122 | \n\t\t> 122 | \n|
IRI2012 | \n\t11.3 | \n\t12.2 | \n\t19.0 | \n\t18.3 | \n
Klobuchar | \n\t49.7 | \n\t45.5 | \n\t37.8 | \n\t37.3 | \n
NeQuick2 | \n\t14.0 | \n\t16.9 | \n\t18.6 | \n\t11.5 | \n
NTCM | \n\t25.0 | \n\t25.4 | \n\t24.6 | \n\t32.9 | \n
Amount of cases the models were identified as the best one according to the solar flux ranges.
\n\t\t\tRegion\n\t\t | \n\t\t\n\t\t\tPortion of cases [%]\n\t\t | \n\t|||
\n\t\t | \n\t\t\tF10.7 Range [sfu]\n\t\t | \n\t|||
0 – 82 | \n\t\t83 – 100 | \n\t\t101 – 122 | \n\t\t> 122 | \n|
Whole globe | \n\t28.9 | \n\t41.0 | \n\t51.7 | \n\t59.7 | \n
EU region | \n\t77.8 | \n\t88.8 | \n\t89.3 | \n\t92.2 | \n
USA region | \n\t56.0 | \n\t69.0 | \n\t73.2 | \n\t81.1 | \n
Amount of cases for which the analysis was able to decisively identify the best model.
One of the constrains of this research is the small amount of solar radio flux sub-groups. In our case, the same model is marked as the best one for particular location and time for both F10.7 of 83 sfu and 100 sfu. A finer solar flux scale would be more adequate. We used wide solar flux ranges to keep amount of days in data groups high enough. However, there are still 4 groups with number of days lower then 10 (one group with only 1 day) which we consider to be insufficient. Future research can overcome this issue by including more years into the analysis, preferably a whole solar cycle.
Considering Table 2 and 3, the Klobuchar and NTCM were marked as the best models in more cases than the IRI and NeQuick. Such results are not in agreement with results from [6] and [7] where Klobuchar always performs worse than the NeQuick. However, in our case, both the IRI and NeQuick are driven by averaged indices while NTCM and Klobuchar by daily indices. This provides the advantage for NTCM and Klobuchar of ability to respond on any rapid day-to-day variation of the ionosphere. In the studies [6] and [7] the NeQuick is driven by Ionization level, while we used monthly mean F10.7. It can be expected that applying Ionization level would significantly change our results, this will be done in future.
Good performance of the Klobuchar model in our test is surprise and it will be better investigated in the future work using larger database of reference data, different indices to drive the models and comparing results for different reference data sources.
The Table 4 shows that we were able to decisively identify the best model for most of the cases in the EU and USA region, especially during the middle and high solar activity. This is caused by the fact that during the periods with higher solar activity the difference between modeled TEC and the CODE\'s TEC rises while CODE RMS error stays roughly the same. In particular for these cases the information about the best model can be very important to minimize the potential impact of the ionosphere mismodeling in single frequency positioning. However, to verify this assumption the results should be tested on real TEC measurements.
We compared TEC data modeled by empirical ionospheric models: IRI2012, Klobuchar, NeQuick2 and NTCM to the CODE TEC data. We analyzed CODE GIMs for every two hours for years 2010, 2011 and 2012. The results show that the CODE RMS error values are low enough to identify the decisively best model in most cases above Europe and North America, especially during the days with higher solar radio flux. The ability to decisively recognize the best model decreases for lower solar radio flux values. For these periods more models have mean absolute TEC deference lower than corresponding mean CODE RMS error. The study shows that the Klobuchar and NTCM were marked as the best model in more cases than NeQuick 2 and IRI 2012. However, the performance of all models varies according to the time, location and solar flux which indicates that there is not one model which performs the best under all conditions. In addition, there is still a significant portion of cases for which the best model could not be identified decisively.
In the future work, we plan to analyze data for more years, improve the solar radio flux resolution and include the Galileo version of the NeQuick into our analysis. We also plan to perform the analysis on the different reference databases and test the results on real TEC measurements.
Pavel Najman\'s research work is undertaken in the scope of the TRANSMIT ITN, funded by the Research Executive Agency within the 7th Framework Program of the European Commission, People Program, Initial Training Network, Marie Curie Actions-GA no 264476.
We would like to thank to Astronomical Institute of the University of Bern for freely available CODE maps. We would also like to thank to Bruno Nava and Sandro M. Radicella for the NeQuick 2 source code.
The liver is the major organ metabolizing xenobiotics and endogenous molecules in order to maintain metabolic homeostasis in the organism, which is why it is a target of many toxic substances that cause dysregulated hepatic homeostasis. One of the mostly found clinical liver diseases is nonalcoholic fatty liver disease (NAFLD) (Figure 1) [2, 3]. In NAFLD, hepatocytes get filled up with triglycerides, liver expands and its normal functions may get altered. Although it is a disease, the triglyceride accumulation can still be reversed and normal functions may be restored by proper nutrition and exercise. If these lifestyle changes are not pursued, the damage goes on and results in inflammation followed with fibrosis which is unfortunately irreversible.
\nMolecular mechanisms explaining the hepatoprotective effect of food bioactives. Development of NAFLD/NASH is induced by different risk factors, such as Western-type diet, physical inactivity, and genetic predisposition. In the presence of obesity and IR, there is an increased flux of FFAs to the liver. These FFAs are stored as TG in lipid droplets leading to hepatic fat accumulation or undergo β-oxidation increasing oxidative stress and the inflammatory pathway. The damaged hepatocyte leads to a further increase of inflammatory signaling (IL-1, TNFa, IL-6) and the recruitment of circulating and residual macrophages (KCs). All of these mechanisms can directly induce the activation of HSCs, the major cell type involved in extracellular matrix deposition and liver fibrosis. The bioactive compounds may exert beneficial effects on NAFLD development and progression by inhibiting lipogenesis, β-oxidation of FFAs, inflammation, and HSCs activation. In the cartoon, we have listed the food bioactives indicating the putative mechanisms by which they may improve liver damage in NAFLD [1].
The liver is made up of hepatocytes, Kupffer cells, liver sinusoidal endothelial cells, pit cells, and hepatic stellate cells (HSC) [4]. Activation of stellate cells by injury caused by many etiological factors would lead to cirrhosis, and it would mark the end stage of progressive fibrosis [5]. Oxidative stress has a vital part in establishing fibrosis and consequently cirrhosis [6]. For this reason, using molecules with antioxidant properties has been proposed as a treatment for not only fibrosis but also oxidative stress-related cirrhosis. Liver diseases are considered a major medical problem worldwide. There are known to be a large number of liver diseases caused by different insults. Furthermore, the disease type depends on lifestyle factors. For example, the main causes of liver diseases are reported to be viral and parasitic infections in regions like Africa and Asia. For Europe and America, alcohol consumption is thought to be the most important cause of this disease. However, viral hepatitis has showed an increase in recent times in most of the countries [7]. Lifestyle and unhealthy diet is the leading cause of liver diseases in almost all western countries. Until today, no medication is approved for the treatment of this disease; however, improving diet habits and physical exercise works if the disease is not accompanied by inflammation. On the other hand, biologically active food compounds that regulate gene expressions in lipogenesis, fibrosis, and inflammation serve as good therapeutic means to ameliorate these pathological states observed in liver [1] (Figure 1).
\nOxidative stress is recognized as a disproportion between the production of free radicals (FR) and the antioxidant defenses [8]. Increased levels of prooxidants result in damage to the cell in terms of lipid peroxidation as well as oxidative DNA damage and thus protein damage [9]. One or more unelectrified FR atoms or molecules may be present as radical cations or radical anions. They are usually unstable and highly reactive because they can react with molecules and abstract electrons. Oxygen can reduce and produce reactive oxygen species (ROS) with exciting electrons, secondary to the interaction of transition metals or by the addition of energy [9, 10]. Oxidative stress causes fibrogenesis by increasing transforming cytokines including transforming grown factor-beta-1 (TGFβ1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFα) [3]. Disruption of the liver metabolism arises from increased quantity of ROS to amplified electron transfer in mitochondrial B-oxidation and increased expression and activity of Cyp2el that is from CYP450 family [11]. Intense production of Cyp2e1 is present because of much more consumption of ethanol which is produced by virtue of a lot of direct and indirect mechanisms [12, 13, 14] (Figure 2).
\nMechanisms of enhanced ROS production during hepatocyte damage. Ethanol metabolism promotes strong ROS production in the ER by the inducible CYP. It impairs GSH import in the mitochondria, preventing ROS removal. It also impairs B-oxidation promoting lipid accumulation. ETOH induces lipid-raft clustering and increases iron uptake, promoting Fe2+ leakage from lysosomes and increased Fe2+ loads in mitochondria and ER, resulting in ROS production. Ethanol also reduced the autophagic removal of damaged cellular components. Viral infection challenges the ER protein folding process leading to ROS production and Ca2+ leakage in the cytosol and mitochondria. Increased MAMs formation promotes Ca2+ efflux from ER into mitochondria, increasing mitochondrial ROS production [15].
Cells produce FR as a result of metabolic events; however, this is not the only source that can cause oxidative stress in body. The pollutants in the environment such as toxic chemicals as well as radiation cause a significant increase in amount of FR, ROS, and reactive nitrogen species (RNS) [10]. In the body, variety of different cell types and chemical reactions produce ROS, the most important metabolism is the cytochrome P450 metabolism and mitochondria-catalyzed electron transport reactions. Most of the inflammatory conditions are also responsible from ROS production, and important cell types in these processes are neutrophils, eosinophils, and macrophages [16, 17]. The chief molecule responsible for the reduction of oxygen in mitochondria is ubisemiquinone. Mitochondria is such an important organelle to produce ROS and hydrogen peroxide (H2O2) as it produces 2–3 nmol of superoxide/min per mg of protein, [17]. Different tissues of mammals and different species of mammals have an enzyme called xanthine oxidase, an enzyme belonging to molybdenum, iron-sulfur, flavin hydroxylases that play an important role in the hydroxylation of purines by the oxidation of hypoxanthine to xanthine. Resultant xanthine then oxidized to uric acid. Oxygen reduction takes place in both of these reactions and the first one produces O2−, while the second one produces H2O2 [16]. Inflammation serves as another source of ROS generation. During inflammation, activated macrophages increase their oxygen uptake, and this process results in production of O2−, nitric oxide (NO), and H2O2 [18]. Another mechanism of O2− production during inflammation is by neutrophils; the enzyme nicotine adenine dinucleotide phosphate [NAD(P)H] oxidase generates O2− that is used to destroy bacteria and this nonphagocytic NAD(P)H oxidases produce O2− in a range of 1–10% [19]. Cytochrome P450 (CYP) enzymes are also important in the production of ROS by the breakdown and/or uncoupling of the P450 catalytic cycle. Hyperoxia would trigger 80% of the H2O2 synthesis by microsomes, and under normoxic conditions, peroxisomes produce H2O2 but not O2−, and most of the peroxisomal H2O2 production takes place in liver [16]. Arginine is reduced to citrulline in a five-electron oxidative reaction by nitric oxide synthases (NOSs) and this reaction gives rise to NO. Immune cells can also produce NO in the oxidative burst during inflammation. NO can react with oxygen and water in an extracellular environment in order to form nitrate and nitrite anions. Also, the NO and O2− can react together and cause a more reactive FR called peroxynitrite anion (ONOO−) which can cause lipid peroxidation and fragmentation of DNA [20].
\nAntioxidants are molecules that can help prevent or delay oxidation of an oxidizable substrate when in low concentrations and they have a high affinity to FR [21]. Antioxidants play an important role to maintain health of the organism by scavenging FR by donating electrons to it. This reduces the reactivity of FR and helps maintain prooxidant/antioxidant balance in cell. A lot of different molecules that have antioxidant activity have been identified. Different natural compounds have so far been studied extensively especially in liver diseases (Table 1).
\nAntioxidant | \nMain clinical effects | \nClinical relevance | \n
---|---|---|
Curcumin | \nAntioxidant | \nNo studies available in human hepatic disorders | \n
Antifibrotic | \n||
Anti-inflammatory | \n||
Antimicrobial | \n||
Wound healing | \n||
Anticarcinogenic | \n||
Resveratrol | \nAntioxidant | \nCurrent data are conflicting, so more clinical studies are needed | \n
Anti-inflammatory | \n||
Anticarcinogenic | \n||
Lipid modulation | \n||
Antifibrotic | \n||
Coffee | \nAntinecrotic | \nInverse relationship between coffee-cirrhosis has been demonstrated, but more basic research and prospective clinical trials are necessary | \n
Antifibrotic | \n||
Antioxidant | \n||
Anticholestatic | \n||
Chemoprotective | \n||
Quercetin | \nChelation of transition metal ions | \nNo studies available in human hepatic disorders | \n
Anticarcinogenic | \n||
Cardioprotective | \n||
Bacteriostatic | \n||
Antioxidant | \n||
Antifibrotic | \n||
Anti-inflammatory | \n||
Antiapoptotic | \n||
Antiaggregatory | \n||
Vasodilating | \n||
Silymarin | \nAntioxidant | \nSilymarin has been shown to be effective, but it is necessary to do more clinical trials focused on survival rates of patients with cirrhosis | \n
Antifibrotic | \n||
Anti-inflammatory | \n||
Anticarcinogenic | \n||
Immunomodulation | \n||
Naringenin | \nAntioxidant | \nNo studies available in human hepatic disorders | \n
Hypocholesterolemic | \n||
Anti-estrogenic | \n||
Hypolipidemic | \n||
Antihypertensive | \n||
Anti-inflammatory | \n||
Antifibrotic | \n||
Anticarcinogenic | \n||
Antiatherogenic | \n||
Green tea | \nAnti-inflammatory | \nMore clinical studies are needed | \n
Antiarthritic | \n||
Antimicrobial | \n||
Antioxidant | \n||
Neuroprotective | \n||
Antidiabetic | \n||
Antiangiogenesis | \n||
Anticarcinogenic | \n||
L-carnitine | \nChelation of transition metal ions | \nMore clinical studies are needed | \n
Antioxidant | \n||
Cardioprotective | \n||
Neuroprotective | \n||
Anti-inflammatory | \n||
Lycopene | \nAntioxidant | \nMore clinical studies are needed | \n
Anti-inflammatory | \n||
Chemoprotective | \n||
Anticarcinogenic | \n
Nutritional antioxidants.
Curcumin, diferuloylmethane or 1,7-bis (4-hydroxy-3-methoxyphenyl)1,6-hepadieno-3,5-dione is obtained from the rhizomes of Curcuma longa (turmeric). Curcumin has many pharmacological properties as it is a strong antioxidant, antifibrogenic, anti-inflammatory, antimicrobial, and anticarcinogenic agent and it also aids in a wound healing [22]. The Food and Drug Administration (FDA) has classified turmeric as a safe substance and toxicity assays done on animals have shown curcumin to be safe even when used in high doses. On the other hand, prolonged high-dose intake of turmeric has been associated with incidences of hepatotoxicity in mice and rats [3]. Curcumin is known to have low bioavailability when administered orally. Arcaro et al. [23] used piperine (inhibitor of hepatic and intestinal absorption) together with curcumin. Even in the presence of piperine, antidiabetic and antioxidant activity of curcumin was not altered. But when higher dose of piperine (40 mg/kg) was used, the beneficial effects of curcumin vanished. On the other hand, Sehgal et al. [24] showed the effect of piperine on curcumin in benzo(a)pyrene toxicity in the liver. They found that pretreatment with 100 mg/kg of curcumin protects against a single dose of benzo(a)pyrene; and at this dose, coadministration of piperine had a much better effect than did curcumin alone showing enhancer activity of piperine. In acute and chronic liver injury, curcumin has been shown to have hepatoprotective effects [25]. In 2007, Reyes-Gordillo et al. [26] showed that curcumin is able to inhibit the release of TNF-α, IL-1B, and IL-6. Additionally, curcumin reduces carbon tetrachloride (CC14)-mediated oxidative stress inactivating the nuclear factor-kB (NF-kB) pathway. Moreover, curcumin’s hepatoprotective effect takes place by its interactions with Fe3+ and Cu2+. A study by Jiao et al. [27] suggested that curcumin could serve as an iron chelator since transferrin receptor 1 and iron regulatory proteins, indicators of iron depletion, showed an increase with curcumin administration. Charoensuk et al. [28] have indicated that curcumin increases antioxidant capacity of cells by increasing mRNA and protein levels of factors and enzymes such as nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase (HO-1), NAD(P)H quinone oxidoreductase 1 (NQO1), glutamate cysteine ligase (GCL), transcription factor-3, peroxiredoxin 3 (Prdx3), and Prdx6. Curcumin also increases the activity of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) activity [29, 30]. Curcumin also interacts with enzymes or genes that are important in liver cirrhosis. Hassan et al. [31] showed that curcumin modulates miRNA 199 and 200 which are associated with liver fibrosis in CC14-induced experimental fibrosis model and that curcumin reduced these miRNAs levels close to their basal levels. Finally, in alcohol-induced liver damage, curcumin inhibits the activity of cytochrome P450 2E1 (Cyp2e1) and also its protein levels [32].
\nThe phytoalexin resveratrol (3,5,4′-trans-trihydroxystilbene) is a polyphenol mostly found in red grapes, red wine, peanuts, and berries [33]. Resveratrol has effects on lipid metabolism, and it also has antioxidant, anti-inflammatory, anticarcinogenic, and antifibrogenic properties [34]. The rate of absorption of resveratrol is about 75% following an oral administration [35]. Resveratrol is metabolized to resveratrol sulfate, and in its low concentrations, it is converted into resveratrol glucuronide [36] by enzymes glucuronosyltransferase (UGT) or sulfotransferase (ST) [37]. In 2007, Chávez et al. [34] showed that under CCl4, resveratrol decreased cytokine TGF-β levels and prevented hepatic fibrosis. It also inhibited NF-kB translocation to the nucleus. Resveratrol, as an antioxidant, has protective effects against ethanol-induced lipid peroxidation, toxicity by acetaminophen (APAP), and oxidative stress in animal models of cholestasis [38]. Important player in resveratrol’s antioxidant activity is suggested to be run by the OH groups [7]. Blocking OH group methylation showed that resveratrol and trimethylated resveratrol provide some degree of protection, but the latter one has a better protective effect [39]. Another hepatoprotection mechanism of resveratrol comes from its ability to activate genes related to antioxidant system or from its ability to inhibit enzymes. A study by Cheng et al. [40] suggested that resveratrol could activate extracellular signal-regulated kinase (ERK) signaling pathway, which may, in turn, enhance the activation and translocation of Nrf2 to the nucleus, thus increasing the expression of HO-1 and glyoxalase. Price et al. [41] found that resveratrol activates AMP-activated protein kinase (AMPK) and increased nicotinamide adenine dinucleotide (NAD) levels in mice. Zhu et al. [42] have also shown that, in mice, administration of resveratrol increased the antioxidant system (SOD, GPx, and GSH) and also the levels of SIRTI and p-AMPK were upregulated in liver. Resveratrol has also been shown to inhibit the activity of Cyp2e1 in microsomes of rat liver [43]. Resveratrol also inhibited the activity of P450 isoform APAP-induced liver injury model [44] and activity of Cyp2e1 was also inhibited in diethylnitrosamine (DEN)-induced hepatocarcinogenesis model [45]. The only clinical study that was performed to determine the resveratrol hepatoprotective effect demonstrated that a 500 mg resveratrol dose administrated for 12 weeks caused a significant reduction in inflammatory cytokines, serum cytokeratin-18, NF-kB activation, liver alanine aminotransferase (ALT), and hepatic steatosis when compared to the placebo group in patients with nonalcoholic fatty liver disease (NAFLD) [46].
\nCoffee is a mixture of several different molecules such as carbohydrates, vitamins, lipids, nitrogenous molecules, alkaloids, and phenolic compounds [47]. Caffeine, diterpene alcohols (cafestol and kahweol), and chlorogenic acid are the three major compounds found in coffee [48]. Coffee consumption has been linked to the reduction of several chronic diseases [49], probably due to the pharmacological properties that have antinecrotic, antifibrotic, anticholestatic, chemoprotective, and antioxidant functions [50]. Caffeine is the best-known active component of coffee, which is absorbed very rapidly once it has been taken orally (5 min), reaching its peak blood levels after 30 min. When consumed in high amounts, it may produce some side effects. Recommendations from Health Canada in 2013 demanded that the daily caffeine intake for children should not exceed 2.5 mg/kg of the body weight. What is more, tachycardia and arrhythmia typically arise when more than 200 mg of caffeine are ingested [51]. Smith et al. [52] reported in 2002 that the intake of 300 mg of caffeine resulted in a rise in anxiety and tension. Caffeine gets metabolized in the liver. The principal metabolite of caffeine is paraxanthine [53]. An important property of caffeine is that it can easily pass through the blood-brain barrier [54]. Coffee-cirrhosis relationship was shown by Klatsky et al. for the first time [55]. The study showed that the odds ratio for liver cirrhosis tend to decrease from 1.0 for people abstaining from coffee to 0.47, 0.23, 0.21, and 0.16 for 1, 2, 3, or 4 cups of coffee daily, respectively. Although coffee is generally beneficial to the liver, this study failed to show a causative role of coffee in prevention of liver injury. Therefore, additional basic research and controlled prospective studies are needed in order to show exact effect of coffee on liver tissue. Arauz et al. [50] demonstrated that coffee has a protective effect upon liver injury caused by chronic administration of thioacetamide (TAA). Coffee ameliorated cholestasis and necrosis and this was seen by the measurement of γ-glutamyl transpeptidase (γ-GTP), alkaline phosphatase, and ALT levels. Arauz et al. [50] demonstrated in murine models that coffee prevents experimental liver cirrhosis. In these studies, coffee reduced the expression of the profibrogenic cytokine TGF-β. Cavin et al. [56] reported coffee to be an inductor of GST, aldo-keto reductase, GSH, HO-1, GST-P1, which are enzymes involved in the detoxification process. Also, they suggested that a possible mechanism of chemoprotection of coffee by stimulating the Nrf2 pathway. In another study, coffee was able to elevate mRNA levels of NQO1 and glutathione-S transferase Al in the liver and the small intestine [57].
\nQuercetin, 3,3,4,5,7-penta-hydroxyflavone, is a flavonol especially found in apples and onions [58]. Quercetin chelates heavy metals and has anticarcinogenic, cardioprotective, bacteriostatic, anti-inflammatory, and antioxidant properties [59]; it also functions as a hepatoprotective agent [60]. The normal daily intake of quercetin is less than 5–40 mg. However, if the peels of the foods that contain high amount of quercetin are also consumed, daily intake of quercetin increases to 200–500 mg [59]. In 2004, high-purity quercetin used in foods was grass that serves 10–125 mg of quercetin [59]. The functional groups responsible for quercetin’s antioxidant activity were described by Bors et al. [61] in 1990, and they found that orthodihydroxy or catechol groups in the B-ring, a 2,3-double bond of the C-ring, and OH substitution on positions 3 and 5 of the C-ring and A-ring, respectively, are important players in antioxidant action of quercetin [61]. It can interact with both FR and metal ions like Fe3+ and Cu2+ for chelation. In a study by Mira et al. [62], it was reported that reduction of Fe3+ and Cu2+ takes place by quercetin’s 2,3-double bond and the presence of catechol group in the B-ring. Following ingestion, quercetin is rapidly absorbed and its levels in blood peak at approximately in 30 min [63] before it is metabolized by glucuronidation and sulfation by the UGT and ST, respectively.
\nIn experimental fibrosis model in rats, quercetin showed hepatoprotective properties under CCl4 treatment that lasted 8 weeks. The hepatoprotective effect of quercetin was found to be mediated by its ability to suppress the expression of profibrogenic expressions of TGF-β, CTGF, and collagen-lα (Col-1α). On the other hand, quercetin also activated enzymes such as metalloproteinases 2 and 9 (MMP2 and MMP9); it also improved the activity of SOD and CAT [64]. Pavanato et al. [65] extended CCl4 treatment for 16 weeks and also observed that quercetin improved the hepatic liver enzymes AST, ALT, and inducible NOS (INOS) expressions; it also decreased collagen amount and reduced lipid peroxidation in liver. Granado-Serrano et al. [66] showed that quercetin modulated Nrf2 and p38 in HepG2 cells. Quercetin has also been shown to suppress the activity of Cyp2e1 in hepatocytes in the presence of ethanol [67]. In line with this finding, in a nonalcoholic steatohepatitis (NASH) model, quercetin was able to reduce Cyp2el activity [68].
\nSilymarin, milk thistle or Saint Mary’s thistle, is a natural substance obtained from Silybum marianum [7]. Silymarin has not been associated with any side effects at acute consumption and the dose range used in literature ranges between 280 and 800 mg/kg of body weight per day. After oral administration, the silymarin peak plasma concentration is achieved at approximately 6–8 h. The metabolites of silymarin get conjugated in the liver by UGT and ST (phase II reactions) [69]. This substance has many hepatoprotective effects (Figure 3). In fact, silybin, a major constituent of silymarin, has found to have iron chelating properties [71]. In a study performed by Najafzadeh et al. [72], hepatoprotective effect of silymarin in iron-overload-induced hepatotoxicity was attributed to its iron-chelator activity; however, no studies have proved the chelating properties per se of silymarin in liver diseases. Silymarin acts as hepatoprotector against several hepatotoxins including D-galactosamine [73]. Silymarin’s ameliorating effects on oxidative stress, fibrosis, cirrhosis, and lipid peroxidation are modulated by its phosphatidylethanolamine amount [74]. This hepatoprotective effect is seen with the improvement of liver enzyme activities and levels of cholesterol/phospholipids and also sphingomyelin/phosphatidylcholine ratios in the membrane [75, 76]. Kim et al. [77] showed that silymarin increases nuclear translocation of Nrf2 in activated HSC. Also, silymarin increases the activity of antioxidant enzymes such as SOD, GPX [78], and CAT [79]. A clinical trial examining silymarin in a complex with phosphatidylcholine found reduced levels of the liver enzymes, ALT and γ-GGT, and serum bilirubin levels in a dose-dependent manner in patients suffering from hepatitis due to virus infection or alcohol abuse [80] (Figure 3).
\nA schematic notation of the main pharmacological effects of silymarin in accordance with its hepatoprotective features: The effects of Sm upon cell membranes (upper left) and intracellular cascades are shown here. The metabolic paths are indicated by interrupted lines, while its signal effects are shown in full lines. LTB4, leukotriene B4; GSH, glutathione; NF-kΒ, nuclear factor kappa B; PG’s, prostaglandins; Sm, silymarin; SOD, superoxide dismutase; ROS, reactive oxygen types=; TNFa, tumor necrosis factor α [70].
Naringenin is also recognized as 5,7,4′-thihydroxyflavanone, and it is a flavanone found in citrus fruits and tomatoes [81]. In a recent study, Yang et al. [82] have reported that naringenin did not cause any harmful effects in beagle dogs, the maximum time of exposure being 180 days and with doses varying of 20, 100, or 500 mg/kg body weight per day. Naringenin has many pharmacological properties. It acts as a hypolipidemic, antihypertensive, anti-inflammatory, antioxidant, and antifibrotic agent [81]. The metabolism of naringenin takes place in small intestine where glycoside form of naringenin gets cleaved, resulting in sulfate and glucuronide metabolites in the small intestine wall; then, it gets absorbed [77]. Mira et al. [62] showed that naringenin can reduce Fe3+ and Cu2+ ions but it is less potent than quercetin. Chtourou et al. [83] found that naringenin averts depletion of SOD, CAT, GPx, and GSH. On the other hand, naringenin also prevents an increase in lipid peroxidation, and it also prevents increase of enzymes ALT and AST [78]. Yen et al. [84] also obtained similar results on liver enzymes and prevention of lipid peroxidation when they used naringenin alone and also naringenin-loaded nanoparticle system (NARN). In both treatments, naringenin exhibited antioxidant and hepatoprotective activities. In these experiments, treatment with naringenin also inhibited the activation of caspases 3 and 8. However, NARN was found to have better hepatoprotective and antioxidant effects than free naringenin, and it was also shown to inhibit caspase 9 during CC14-induced hepatotoxicity in rats. Han et al. [64] reported that a pretreatment with naringenin-7-O-glucoside increases NQO1 and ERK phosphorylation and translocation of Nrf2 to the nucleus in H9c2 cardiomyocytes. It also upregulated the mRNA expression of GCLC and GCL modifier [64]. Similar findings have been reported by Esmaeili et al. [85] who showed that naringenin attenuates CC14-induced liver injury by downregulating TNF-α, INOS, and cyclooxigenase-2 and also by increasing Nfr2 and HO-1 expressions. Motawi et al. [86] showed that naringenin inhibits Cyp2e1 in liver microsomal assay done on rats [86].
\nCamellia sinensis or green tea is a widely consumed beverage across the globe and it has antioxidant, anti-inflammatory, antiarthritic, and antiangiogenic effects. It is a mixture of polyphenols (the major class of active compounds) including catechins (also known as flavan-3-ols) which constitute about 30% (mass fraction) of green tea leaves. The major catechins in green tea are (+) -catechin, (−) -epicatechin, (−) -epigallocatechin, (−) -epicatechin-3-gallate, (−) -gallocatechin, (−) -gallocatechin gallate, and (−) -epigallocatechin-3-gallate (EGCG). EGCG is the most abundant catechin accounting for 50% of total polyphenols; thus, it is the main biological active compound of green tea [87]. However, polyphenols are not the only compounds that green tea exerts its antioxidant activity with through. The amino acid, L-theanine, in green tea accounts for 1–2% of the leaf dry weight that is synthetized in the roots of green tea and is concentrated in the leaves. Studies have reported that L-theanine protects the cell by maintaining its GSH levels in cancer and neurotoxic diseases [88]. The intake of green tea can be considered safe unless its consumption exceeds 1–2 cups a day. And higher consumption such as in attempts to lose weight resulted in hepatotoxicity [87]. At normal doses, Pérez-Vargas et al. [88] found that the main amino acid of green tea, L-theanine, reduced expression of NF-kB and downregulated IL-1β and IL-6 and the cytokines TGF-β and CTGF. Halegoua-De Marzio et al. [89] tested a single high dose of green tea (400 mg), in patients with HCV-induced cirrhosis and found that it is well tolerated by patients and beneficial for treating cirrhosis.
\nL-Carnitine (LC), B-hydroxy-y-trimethylaminobutyric acid, is a water-soluble molecule important in mitochondrial oxidation of fatty acids in mammalian metabolism (Figure 4). LC can exist in three different forms: as free LC, acetyl-L-carnitine (ALC), or other carnitine esters. About 25% of carnitine is obtained from methionine biosynthesis, but most LC is provided by the diet, especially through red meat and milk consumption [91]. LC acts as a carrier of fatty acids across the inner mitochondrial membrane for β-oxidation and ATP production. Apart from its role in the lipid metabolism, LC is also a potent antioxidant, and it protects tissues from oxidative damage. Reduced concentrations of LC in the body are mostly due to the accumulating toxic metabolites and also because of lack of protein in restricted diets. Thus, LC supplementation could be useful not only to supply the tissues in presence of but also in avoiding oxidative damage as a result of increased amounts of reactive species. Since LC can easily cross the blood-brain barrier, LC supplementation may also be beneficial in preventing oxidative injury-related neurological damage and further studies are needed in order to clearly establish LC’s role in neurological diseases [92].
\nThe mitochondrial carnitine system. Abbreviations: CPT I, carnitine-palmitoyl transferase I; CACT, carnitine acyl carnitine transferase; CPT II, carnitine-palmitoyl transferase II; CAT, carnitine acyl transferase; CoA, coenzyme A [90].
Lycopene (LYC) is an acyclic isomer of beta-carotene which has great antioxidant activities. It is synthesized by plants or autotrophic bacteria but not by animals. Red fruits and vegetables, such as tomatoes, watermelons, pink grapefruits, apricots, pink guavas, and papaya, contain LYC. Studies show that LYC consumption not only reduces the risk of cancer of many organs but also retards the growth of tumors. LYC has been shown to have protective effects on other pathologies such as cardiovascular diseases, osteoporosis, male infertility, and this action is mainly mediated by LC’s ability to inhibit other toxic agents (Figure 5). Numerous in vitroand in vivo studies showed that LYC could provide protection against ionizing radiation. Therefore, supplementation of LYC might be protective against damaging effects of radiotherapy in cancer treatments and it can also be protective against accidental radiation exposure [94].
\nGeneral mechanisms of action of lycopene. The proposed mechanisms of action of lycopene (oxidative and nonoxidative) that decreases the risk of oxidative stress-mediated diseases. Lycopene most likely acts via the oxidative mechanism of action to prevent oxidative stress and its detrimental effects on male infertility. ROS: reactive oxygen species [93].
Piperine [1-[5-(1,3-benzodioxol-5-yl)-1-oxo-2,4, pentadienyl] piperidine] is the major pungent alkaloid present in the fruits of Piper nigrum L. [95]. Piperine at low concentrations acts as a hydroxyl radical scavenger, but at higher concentrations, it activates the Fenton reaction, resulting in increased generation of hydroxyl radicals. Piperine has hepatoprotective effects and it was shown to inhibit lipid peroxidation in the rat liver microsomes at a concentration of 600 μM [96].
\nCapsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is the major strong and irritating ingredient of red pepper. It may inhibit copper ion-induced lipid peroxidation of human LDL, which suggests that it is an effective antioxidant offering protection against oxidation of human LDL [97].
\nDiallyl sulfides and diallyl disulfides, the active components of garlic, have anti-inflammatory and antimutagenic activities. Onion is a major source of flavonoids, especially the two quercetin glycosides, quercetin 4-o-β-glucoside and quercetin 3,4-o-β-diglucosides, which are recognized as bioactive substances. In order to show the antioxidant properties and protective effects of garlic and onion, a study was carried out on rats. Animals were treated with 0.6 mg nicotine/kg and also given 100 mg garlic or onion oils/kg for 21 days. Nicotine increased concentrations of thiobarbituric acid, conjugated dienes, and hydroperoxides in the tissues. Supplementation with both the garlic oil and onion oil increased resistance not only to lipid peroxidation but they also increased levels of antioxidant enzymes and glutathione. These conclusions state that oils of garlic and onion are effective antioxidants against nicotine-related oxidative stress and damage [98].
\nVitamin C, substrate for ascorbate peroxidase, is not only a highly effective antioxidant but also an essential component of a healthy diet. Vitamin E, the major antioxidant found in lipid composition of membranes, is a fat-soluble antioxidant. During fat oxidization, vitamin E helps to inhibit formation of ROS [99]. Several studies showed that vitamin E serum levels are significantly reduced in alcoholic liver disease [100]. It is also shown that vitamin E levels are inversely proportional to formation of oxidative stress products that correlate with the extent of liver damage [101]. For this reason, maintenance of normal concentrations of vitamin E appears to be necessary for preventing lipid peroxidation due to alcohol consumption. Works from several laboratories have so far indicated that mitochondrial damage may present a common early event in cell injury [102]. It is possible to prevent mitochondrial damage through vitamin E [103]. Vitamin E or C alone, or in combination, can ease scavenging free radicals that are generated in the liver tissue [104]. In the mouse model, vitamin E supplementation restores alcohol-induced redox status, reduces apoptosis, and prevents oxidative stress [105]. What is more, vitamin E is effective in doses of 600 mg daily when it comes to suppressing HBV replication and normalizing ALT in a significant proportion of chronically infected patients with CLD [106].
\nTrace minerals act as a cofactor of antioxidant enzymes thus enabling the antioxidant activities to take place. These trace minerals include selenium (Se), zinc (Zn), manganese (Mn), iron (Fe), and copper (Cu) [103]. O2− radicals are eliminated by the enzyme Cu-Zn-SOD and Cu and Zn are the co-factors for the enzyme. One of the enzymes responsible for H2O2 clearance from the cells is CAT and Fe is the essential cofactor of this enzyme. Levels of ferritin may decline with exercise and increasing dietary or supplemental Fe can improve performance. It was shown that moderate-level supplementation of Fe to competitive swimmers increased their performance and helped to maintain normal ferritin levels [107]. Selenium (Se) is a cofactor for the antioxidant enzyme GPx, which is like the enzyme CAT, responsible for removing H2O2 and other organic H2O2 from the cell. A study by Akil et al. [108] showed in rats, that upon acute swimming exercise, lipid peroxidation in the brain was increased and Se supplementation to these rats increased antioxidant activity resulting in inhibition of the free radical production [108]. Manganese (Mn) is a cofactor for the enzyme Mn-SOD. It eliminates O2− radicals produced during oxidative phosphorylation [109].
\nInvestigations done on antioxidants have shown that these compounds are candidates for the treatment and candidates to prevent oxidative stress-related diseases. This chapter focuses on antioxidants that can be investigated in experimental and clinical trials of many diseases but especially in diseases of liver. Main nutritional components involved in the production and/or removal of free radicals and the role of free radicals in the pathogenesis of several hepatic diseases and related comorbidities have been described in this chapter.
\nAmong the antioxidants that were described, curcumin, naringenin, and quercetin have been found to be effective antioxidants in treatment of experimental liver injury. Green tea has been shown to protect against different kinds of cancer in clinical trials but not on hepatocellular carcinoma. Resveratrol has been extensively studied in experimental models of liver diseases and has been shown to have protective effects on fibrosis. So far, there are not much clinical trials on ameliorating and disease preventing effects of most potent antioxidants on liver and these antioxidants are good candidates for clinical trials not only because they show great disease preventing and ameliorating effects but also because they are derived from food sources and have a good metabolic tolerance.
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\\n\\nCo-Author: All other Authors of the Chapter besides the Corresponding Author.
\\n\\nIntechOpen: IntechOpen Ltd., the Publisher of the Book.
\\n\\nBook: The publication as a collection of chapters compiled by IntechOpen including the Chapter. Chapter: The original literary work created by Corresponding Author and any Co-Author that is the subject of this Agreement.
\\n\\n2. CORRESPONDING AUTHOR'S GRANT OF RIGHTS
\\n\\n2.1 Subject to the following Article, the Corresponding Author grants and shall ensure that each Co-Author grants, to IntechOpen, during the full term of copyright and any extensions or renewals of that term the following:
\\n\\nThe aforementioned licenses shall survive the expiry or termination of this Agreement for any reason.
\\n\\n2.2 The Corresponding Author (on their own behalf and on behalf of any Co-Author) reserves the following rights to the Chapter but agrees not to exercise them in such a way as to adversely affect IntechOpen's ability to utilize the full benefit of this Publication Agreement: (i) reprographic rights worldwide, other than those which subsist in the typographical arrangement of the Chapter as published by IntechOpen; and (ii) public lending rights arising under the Public Lending Right Act 1979, as amended from time to time, and any similar rights arising in any part of the world.
\\n\\nThe Corresponding Author confirms that they (and any Co-Author) are and will remain a member of any applicable licensing and collecting society and any successor to that body responsible for administering royalties for the reprographic reproduction of copyright works.
\\n\\nSubject to the license granted above, copyright in the Chapter and all versions of it created during IntechOpen's editing process (including the published version) is retained by the Corresponding Author and any Co-Author.
\\n\\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\\n\\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\\n\\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\\n\\n3. CORRESPONDING AUTHOR'S DUTIES
\\n\\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\\n\\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\\n\\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\\n\\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\\n\\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\\n\\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\\n\\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\\n\\n4. CORRESPONDING AUTHOR'S WARRANTY
\\n\\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\\n\\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\\n\\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\\n\\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\\n\\n5. TERMINATION
\\n\\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\\n\\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\\n\\n6. INTECHOPEN’S DUTIES AND RIGHTS
\\n\\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\\n\\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\\n\\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\\n\\n7. MISCELLANEOUS
\\n\\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\\n\\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\\n\\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\\n\\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\\n\\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\\n\\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\\n\\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\\n\\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\\n\\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\\n\\nLast updated: 2020-11-27
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The Corresponding Author (acting on behalf of all Authors) and INTECHOPEN LIMITED, incorporated and registered in England and Wales with company number 11086078 and a registered office at 5 Princes Gate Court, London, United Kingdom, SW7 2QJ conclude the following Agreement regarding the publication of a Book Chapter:
\n\n1. DEFINITIONS
\n\nCorresponding Author: The Author of the Chapter who serves as a Signatory to this Agreement. The Corresponding Author acts on behalf of any other Co-Author.
\n\nCo-Author: All other Authors of the Chapter besides the Corresponding Author.
\n\nIntechOpen: IntechOpen Ltd., the Publisher of the Book.
\n\nBook: The publication as a collection of chapters compiled by IntechOpen including the Chapter. Chapter: The original literary work created by Corresponding Author and any Co-Author that is the subject of this Agreement.
\n\n2. CORRESPONDING AUTHOR'S GRANT OF RIGHTS
\n\n2.1 Subject to the following Article, the Corresponding Author grants and shall ensure that each Co-Author grants, to IntechOpen, during the full term of copyright and any extensions or renewals of that term the following:
\n\nThe aforementioned licenses shall survive the expiry or termination of this Agreement for any reason.
\n\n2.2 The Corresponding Author (on their own behalf and on behalf of any Co-Author) reserves the following rights to the Chapter but agrees not to exercise them in such a way as to adversely affect IntechOpen's ability to utilize the full benefit of this Publication Agreement: (i) reprographic rights worldwide, other than those which subsist in the typographical arrangement of the Chapter as published by IntechOpen; and (ii) public lending rights arising under the Public Lending Right Act 1979, as amended from time to time, and any similar rights arising in any part of the world.
\n\nThe Corresponding Author confirms that they (and any Co-Author) are and will remain a member of any applicable licensing and collecting society and any successor to that body responsible for administering royalties for the reprographic reproduction of copyright works.
\n\nSubject to the license granted above, copyright in the Chapter and all versions of it created during IntechOpen's editing process (including the published version) is retained by the Corresponding Author and any Co-Author.
\n\nSubject to the license granted above, the Corresponding Author and any Co-Author retains patent, trademark and other intellectual property rights to the Chapter.
\n\n2.3 All rights granted to IntechOpen in this Article are assignable, sublicensable or otherwise transferrable to third parties without the Corresponding Author's or any Co-Author’s specific approval.
\n\n2.4 The Corresponding Author (on their own behalf and on behalf of each Co-Author) will not assert any rights under the Copyright, Designs and Patents Act 1988 to object to derogatory treatment of the Chapter as a consequence of IntechOpen's changes to the Chapter arising from translation of it, corrections and edits for house style, removal of problematic material and other reasonable edits.
\n\n3. CORRESPONDING AUTHOR'S DUTIES
\n\n3.1 When distributing or re-publishing the Chapter, the Corresponding Author agrees to credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen. The Corresponding Author warrants that each Co-Author will also credit the Book in which the Chapter has been published as the source of first publication, as well as IntechOpen, when they are distributing or re-publishing the Chapter.
\n\n3.2 When submitting the Chapter, the Corresponding Author agrees to:
\n\nThe Corresponding Author will be held responsible for the payment of the Open Access Publishing Fees.
\n\nAll payments shall be due 30 days from the date of the issued invoice. The Corresponding Author or the payer on the Corresponding Author's and Co-Authors' behalf will bear all banking and similar charges incurred.
\n\n3.3 The Corresponding Author shall obtain in writing all consents necessary for the reproduction of any material in which a third-party right exists, including quotations, photographs and illustrations, in all editions of the Chapter worldwide for the full term of the above licenses, and shall provide to IntechOpen upon request the original copies of such consents for inspection (at IntechOpen's option) or photocopies of such consents.
\n\nThe Corresponding Author shall obtain written informed consent for publication from people who might recognize themselves or be identified by others (e.g. from case reports or photographs).
\n\n3.4 The Corresponding Author and any Co-Author shall respect confidentiality rights during and after the termination of this Agreement. The information contained in all correspondence and documents as part of the publishing activity between IntechOpen and the Corresponding Author and any Co-Author are confidential and are intended only for the recipient. The contents may not be disclosed publicly and are not intended for unauthorized use or distribution. Any use, disclosure, copying, or distribution is prohibited and may be unlawful.
\n\n4. CORRESPONDING AUTHOR'S WARRANTY
\n\n4.1 The Corresponding Author represents and warrants that the Chapter does not and will not breach any applicable law or the rights of any third party and, specifically, that the Chapter contains no matter that is defamatory or that infringes any literary or proprietary rights, intellectual property rights, or any rights of privacy. The Corresponding Author warrants and represents that: (i) the Chapter is the original work of themselves and any Co-Author and is not copied wholly or substantially from any other work or material or any other source; (ii) the Chapter has not been formally published in any other peer-reviewed journal or in a book or edited collection, and is not under consideration for any such publication; (iii) they themselves and any Co-Author are qualifying persons under section 154 of the Copyright, Designs and Patents Act 1988; (iv) they themselves and any Co-Author have not assigned and will not during the term of this Publication Agreement purport to assign any of the rights granted to IntechOpen under this Publication Agreement; and (v) the rights granted by this Publication Agreement are free from any security interest, option, mortgage, charge or lien.
\n\nThe Corresponding Author also warrants and represents that: (i) they have the full power to enter into this Publication Agreement on their own behalf and on behalf of each Co-Author; and (ii) they have the necessary rights and/or title in and to the Chapter to grant IntechOpen, on behalf of themselves and any Co-Author, the rights and licenses expressed to be granted in this Publication Agreement. If the Chapter was prepared jointly by the Corresponding Author and any Co-Author, the Corresponding Author warrants and represents that: (i) each Co-Author agrees to the submission, license and publication of the Chapter on the terms of this Publication Agreement; and (ii) they have the authority to enter into this Publication Agreement on behalf of and bind each Co-Author. The Corresponding Author shall: (i) ensure each Co-Author complies with all relevant provisions of this Publication Agreement, including those relating to confidentiality, performance and standards, as if a party to this Publication Agreement; and (ii) remain primarily liable for all acts and/or omissions of each such Co-Author.
\n\nThe Corresponding Author agrees to indemnify and hold IntechOpen harmless against all liabilities, costs, expenses, damages and losses and all reasonable legal costs and expenses suffered or incurred by IntechOpen arising out of or in connection with any breach of the aforementioned representations and warranties. This indemnity shall not cover IntechOpen to the extent that a claim under it results from IntechOpen's negligence or willful misconduct.
\n\n4.2 Nothing in this Publication Agreement shall have the effect of excluding or limiting any liability for death or personal injury caused by negligence or any other liability that cannot be excluded or limited by applicable law.
\n\n5. TERMINATION
\n\n5.1 IntechOpen has a right to terminate this Publication Agreement for quality, program, technical or other reasons with immediate effect, including without limitation (i) if the Corresponding Author or any Co-Author commits a material breach of this Publication Agreement; (ii) if the Corresponding Author or any Co-Author (being an individual) is the subject of a bankruptcy petition, application or order; or (iii) if the Corresponding Author or any Co-Author (being a company) commences negotiations with all or any class of its creditors with a view to rescheduling any of its debts, or makes a proposal for or enters into any compromise or arrangement with any of its creditors.
\n\nIn case of termination, IntechOpen will notify the Corresponding Author, in writing, of the decision.
\n\n6. INTECHOPEN’S DUTIES AND RIGHTS
\n\n6.1 Unless prevented from doing so by events outside its reasonable control, IntechOpen, in its discretion, agrees to publish the Chapter attributing it to the Corresponding Author and any Co-Author.
\n\n6.2 IntechOpen has the right to use the Corresponding Author’s and any Co-Author’s names and likeness in connection with scientific dissemination, retrieval, archiving, web hosting and promotion and marketing of the Chapter and has the right to contact the Corresponding Author and any Co-Author until the Chapter is publicly available on any platform owned and/or operated by IntechOpen.
\n\n6.3 IntechOpen is granted the authority to enforce the rights from this Publication Agreement, on behalf of the Corresponding Author and any Co-Author, against third parties (for example in cases of plagiarism or copyright infringements). In respect of any such infringement or suspected infringement of the copyright in the Chapter, IntechOpen shall have absolute discretion in addressing any such infringement which is likely to affect IntechOpen's rights under this Publication Agreement, including issuing and conducting proceedings against the suspected infringer.
\n\n7. MISCELLANEOUS
\n\n7.1 Further Assurance: The Corresponding Author shall and will ensure that any relevant third party (including any Co-Author) shall, execute and deliver whatever further documents or deeds and perform such acts as IntechOpen reasonably requires from time to time for the purpose of giving IntechOpen the full benefit of the provisions of this Publication Agreement.
\n\n7.2 Third Party Rights: A person who is not a party to this Publication Agreement may not enforce any of its provisions under the Contracts (Rights of Third Parties) Act 1999.
\n\n7.3 Entire Agreement: This Publication Agreement constitutes the entire agreement between the parties in relation to its subject matter. It replaces and extinguishes all prior agreements, draft agreements, arrangements, collateral warranties, collateral contracts, statements, assurances, representations and undertakings of any nature made by or on behalf of the parties, whether oral or written, in relation to that subject matter. Each party acknowledges that in entering into this Publication Agreement it has not relied upon any oral or written statements, collateral or other warranties, assurances, representations or undertakings which were made by or on behalf of the other party in relation to the subject matter of this Publication Agreement at any time before its signature (together "Pre-Contractual Statements"), other than those which are set out in this Publication Agreement. Each party hereby waives all rights and remedies which might otherwise be available to it in relation to such Pre-Contractual Statements. Nothing in this clause shall exclude or restrict the liability of either party arising out of its pre-contract fraudulent misrepresentation or fraudulent concealment.
\n\n7.4 Waiver: No failure or delay by a party to exercise any right or remedy provided under this Publication Agreement or by law shall constitute a waiver of that or any other right or remedy, nor shall it preclude or restrict the further exercise of that or any other right or remedy. No single or partial exercise of such right or remedy shall preclude or restrict the further exercise of that or any other right or remedy.
\n\n7.5 Variation: No variation of this Publication Agreement shall be effective unless it is in writing and signed by the parties (or their duly authorized representatives).
\n\n7.6 Severance: If any provision or part-provision of this Publication Agreement is or becomes invalid, illegal or unenforceable, it shall be deemed modified to the minimum extent necessary to make it valid, legal and enforceable. If such modification is not possible, the relevant provision or part-provision shall be deemed deleted.
\n\nAny modification to or deletion of a provision or part-provision under this clause shall not affect the validity and enforceability of the rest of this Publication Agreement.
\n\n7.7 No partnership: Nothing in this Publication Agreement is intended to, or shall be deemed to, establish or create any partnership or joint venture or the relationship of principal and agent or employer and employee between IntechOpen and the Corresponding Author or any Co-Author, nor authorize any party to make or enter into any commitments for or on behalf of any other party.
\n\n7.8 Governing law: This Publication Agreement and any dispute or claim (including non-contractual disputes or claims) arising out of or in connection with it or its subject matter or formation shall be governed by and construed in accordance with the law of England and Wales. The parties submit to the exclusive jurisdiction of the English courts to settle any dispute or claim arising out of or in connection with this Publication Agreement (including any non-contractual disputes or claims).
\n\nLast updated: 2020-11-27
\n\n\n\n
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"54525",title:"Prof.",name:"Abdul Latif",middleName:null,surname:"Ahmad",slug:"abdul-latif-ahmad",fullName:"Abdul Latif Ahmad",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"20567",title:"Prof.",name:"Ado",middleName:null,surname:"Jorio",slug:"ado-jorio",fullName:"Ado Jorio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universidade Federal de Minas Gerais",country:{name:"Brazil"}}},{id:"47940",title:"Dr.",name:"Alberto",middleName:null,surname:"Mantovani",slug:"alberto-mantovani",fullName:"Alberto Mantovani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). I am a Reviewer for several refereed journals and international conferences, such as IEEE Transactions on Biomedical Engineering, IEEE Transactions on Industrial Electronics, Optic Letters, Measurement Science Review, and also a member of the International Advisory Committee for 2012 IEEE Business Engineering and Industrial Applications and 2012 IEEE Symposium on Business, Engineering and Industrial Applications.",institutionString:null,institution:{name:"Joseph Fourier University",country:{name:"France"}}},{id:"55578",title:"Dr.",name:"Antonio",middleName:null,surname:"Jurado-Navas",slug:"antonio-jurado-navas",fullName:"Antonio Jurado-Navas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/55578/images/4574_n.png",biography:"Antonio Jurado-Navas received the M.S. degree (2002) and the Ph.D. degree (2009) in Telecommunication Engineering, both from the University of Málaga (Spain). He first worked as a consultant at Vodafone-Spain. 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