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Level 42 Bass Transcriptions Pdf


Ron Carter, the icon of walking jazz bass lines, has now re-invented the way transcriptions are written. The method is called "Chartography" (often misspelled as Cartography)and musicians will be in awe of how much they can learn when studying this completely new innovation.




level 42 bass transcriptions pdf



By looking at how a bass line evolved over multiple choruses and performances, you will understand that a one-chorus transcription cannot help a bass player find out how that bass line was actually built. much less how to write one like it himself.


"A single, one-chorus transcription of a bass line you admire cannot help you learn to do it yourself. But if you understand all the elements and the context that went into creating it, you can up your game and learn to write bass lines like the ones that inspired you." --Ron Carter


"This book is the first of its kind that actually follows the bass line development of a specific song that shows the string bass genius of Ron Carter. Every bass teacher and every bass player must have this magnificent book". -- Wayne Shorter


One of the most talented instrumentalists of all time, it should come as no surprise that Prince was also a fantastic bassist. In fact, his first four albums were basically one-man efforts, with a few guest spots (though he kept bass duties to himself). His slap style owes much to his hero, Larry Graham.


An iconic figure in the bass world, Doug Wimbish forged a formidable reputation during his time with Sugar Hill Records. New York New York is classic Grandmaster Flash. It has a repeated two-bar slapped phrase during the verse, with Doug playing a different fill on the last three beats of the second bar. Check out the sextuplet in the seventh repeat!


Power is a bass anthem in the key of B, which gives it a different sound to the usual slap-friendly keys of E and A. Look out for the three-finger popped chord on the first beat, the double-thumbed 32nd-note figure on beat two and some killer Larry Graham-style octaves at the end of the second bar.


Now that we've given you our list of the top 20 slap bass grooves that every bass player needs to know... it's time to add them to your own repertoire and, most importantly, learn how to incorporate some of these techniques into your own playing.


The Groove Formula In this rhythm-based course, Scott takes you through exactly how you can turbo charge your bass lines, grooves, time-feel and your overall mastery of the bass - with one simple formula!


Join over 15,000 bass players in the worlds leading bass education platform, which is packed with hours of step-by-step courses, live seminars, interviews and much more. click here and grab your 14 day free trial today.


The toxicity of Hg seems to be inversely related to the concentration of Se and directly related to Se/Hg molar ratio, as demonstrated by numerous studies [3, 8, 9]. The organic Se present in ocean fish has been shown to be bioavailable and effective in counteracting MeHg+ toxicity as long as there is a molar excess of Se with respect to the Hg [1, 5]. Several studies have also shown that the Se molecular form has relevance in neutralizing Hg toxicity [9, 10] and that the Se forms present in ocean fish, in particular selenoneine [9, 11, 12], may be more efficient and safe than other Se forms which, furthermore, display a very narrow range between an optimal and a toxic dose. The work by Yamashita et al. [12] is particularly interesting and shows how selenoneine increases the rate of MeHg+ demethylation and its excretion through the organic cations/carnitine transporter-1 (OCTN1). The formation of stable and inert complexes between selenolate and MeHg+ that can be excreted more efficiently than MeHg+ has also been published [13]. Indeed, the consumption of some species of tuna fish that usually have high levels of Hg and high Se/Hg molar ratios has not been linked to cases of Hg intoxication, while pilot whale consumption, with Se/Hg molar ratios below 1, did provoke intoxications in a Faroe Island population [5]. All these studies indicate that the magnitude of the risk of exposure and the severity of Hg intoxication are not predictable by the level of Hg alone, and one must take into consideration the molar ratio between Se and Hg and the Se molecular form.


There are three TrxR isoenzymes in mammals: the cytosolic TrxR1, the mitochondrial TrxR2, and the testis-specific TrxR3 [14, 15]. However, a study on thioredoxin systems by Pacitti et al. [15] has found only two TrxR forms present in fish, the mitochondrial TrxR2 and an ancestral TrxR3, from which the authors hypothesize that the vertebrate cytosolic TrxR1 and testis-specific TrxR3 likely evolved via a gene duplication event. Interestingly, the same work also showed the presence of two thioredoxin reductase 3 (txnrd3) and another two thioredoxin 1 (txn1) gene isoforms in rainbow trout whose transcription levels varied depending on the tissue and were modulated by exposure to Se compounds and to exposure to infectious agents [15].


Given the scarcity of studies on the mechanism of action of MeHg+ ingestion on the selenogene expression of commercially relevant species, this research was undertaken with the main purpose of generating novel knowledge on such effect on European sea bass. Moreover, since the natural diet of carnivorous fish is other fish and the detoxifying effect of Se is dependent on the Se molecular forms (which may vary from one species to another) [12], we found interesting to examine the potentially mitigating effect of white fish ingestion on MeHg+ toxicity on European sea bass. As mentioned above, the positive effect of pelagic fish on MeHg+ toxicity has been well-documented [9, 11, 12], but that is not the case for white fish, and although adult European sea bass prefer small pelagic fish [24], it would forage on any small fish, including small hake when along the coast. Similarly, as mentioned above, the middle- and long-terms effects of Hg compounds on reductase activities and selenogene transcription have been previously documented, but we were mostly interested in documenting the effect of a short-term contamination, i.e., the response of these systems during the early stages of an accidental contamination taking into account the Se/Hg molar ratio of their feed.


Accordingly, our hypotheses were (1) that the ingestion of MeHg+ affects relevant biomarkers (in particular related to fillet trace element composition, hepatic reductase activities, and selenogene transcription) in the European sea bass and (2) that the substitution of 20% of the feed with a white fish (hake) would mitigate the effects provoked by MeHg+.


The experimental design was carried out in accordance with the EU Directive (2010/63/EU) for animal experiments. It was performed on European sea bass (Dicentrarchus labrax) and had been approved by the Ethical Committee for Animal Welfare (No. CEEA/039/2015).


The fold change in the transcription levels of the four redox genes txn1, gpx1, txnrd3, and txnr2 in Phase A is shown in Fig. 2a, b, c, and d, respectively. As was the case for the reductase activities, the correlation between the transcription of the genes and the Hg in the feed was negative considering the four groups together (Table 3). However, the median values for the transcription of the hepatic selenogenes in A2, fed as A1 an excess of Se over Hg, were higher than that of A1 for txn1 and gpx1, and it was only slightly different for txnrd2 and txnrd3 (Fig. 2). Under an excess of Hg, on the other hand, the transcriptions of all the genes were downregulated (Fig. 2).


No mortality was registered in Phase B, and the three experimental groups, B1, B2, and B3, had significantly increased their weight by the end of the experiment (Table 1). Interestingly, the SGR and final CF were slightly higher in the group receiving both Hg and TH and lowest in the group receiving commercial feed and Hg, indicating a small but positive effect of the inclusion of raw fish in the diet of the sea bass on fish growth. It must be remarked again that the SGRs of Phases A and B are not directly comparable, because the growth rate of smaller individuals (Phase A) is usually different than that of larger fish and because the experimental setup and the lengths of time over which the SGR were calculated are different. The apparent lack of a statistically significant effect of MeHg+ intake on fish growth during Phase B further confirms the results of Stefansson et al. [32], who only noted a slight decrease in fish weight after 70 days of exposure.


The transcription levels of txn1, gpx1, txnrd3, and txnrd2 in Phase B are shown in Fig. 2 and in Table 5 and follow the same pattern as in Phase A for fish fed diets with a molar excess of Hg over Se: exposure to high Hg ratios downregulated txn1, txnrd3, and txnrd2 and upregulated gpx1. With respect to B1, the downregulation in the transcriptions of B2 was in general less severe than in B3 (Table 5), indicating a protective effect of the inclusion of TH in the diet of these fish. The upregulation of gpx1 in both groups may indicate complementarity among selenogenes from the antioxidant pathways. The glutathione system, particularly glutathione reductase, has been reported to complement reduced Trx and TrxR activities in the liver of zebra seabreams during Hg exposure [35]. Although that study did not examine the mRNA levels, our results support that complementarity at the transcriptional level by the negative correlation between the (lowered) activity of both reductases (Fig. 1c, d) and the (upregulated) transcription of gpx1 (Fig. 2g).


The slightly different transcription levels of txnrd3 and txnrd2 may be a reflection of the different responses of the genes coding for the cytosolic and mitochondrial TrxR isoenzymes, respectively. Our results show that the mRNA levels of txnrd3 were slightly increased upon Hg exposure compared to txnrd2, which is similar to the observations of Branco et al. [23]. This indicates a differential effect of MeHg+ on the transcription of the genes coding for TrxR isozymes which differ in location within the cell. The downregulation in the transcription of tnx1 and txnrd2 in B2 is parallel to the decrease in the total DNTB-reductase and TrxR activities of the group (Figs. 1and 2), indicating a net Se deficiency in these individuals. 350c69d7ab


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