simultaneously elevated. Neither elevated saturated fatty acid concentration is negated by the expression of the other saturated fatty acid in the elevated concentration. The endogenously formed palmiticacid content is from about 14% to about 24% and the endogenously formed stearicacid content is from about 20% to about 30% by weight of the total fatty acid composition. In a preferred embodiment, the endogenously formed linolenic acid (C18:3) component of the soybeanoil is no more than about 3% by weight of the total fatty acid composition.
In this study, two-component systems of oleic acid- palmiticacid and palmiticacid- pentadecanoic acid (stearicacid can be used instead of pentadecanoic acid) are used which have the benefits of ease of access, lack of adverse environmental effects and human health, recyclability and reuse or the use of waste as a raw material of this work in
Methods are described for the production of soybean varieties and lines exhibiting linolenic acid contents of less than about 2.5% of the total fatty acid composition as determined by gas chromatography, preferably less than about 2.2% and, more preferably, less than about 1.9%, and in one aspect of the invention, soybean varieties and lines having the low linolenic acid characteristic and a stearicacid content of at least 20%, preferably at least 25%, and, more preferably, at least about 30%, and in a further aspect, soybean varieties and lines having the low linolenic acid content and a palmiticacid content of at least 11%, more preferably at least about 13 or 14%. In accordance with still further aspects of this invention, soybean lines are provided which exhibit a low linolenic acid content and an oleic acid content of at least about 60% of the total fatty acid composition, such lines may, if desired, also contain a palmiticacid content of less than about 6.0% and/or a stearicacid content of less than about 3.5%. There is also disclosed soybean lines having low linolenic acid contents and a palmiticacid content of less than about 5.0%, preferably less than about 4.0%.
Locations showed homogenous error variances for all traits examined allowing for a combined analysis of both locations. The ANOVA revealed significant variation (P < 0.001) among genotypes within each population for all ten traits measured. Location effects were significant (P < 0.05) for linolenic acid content, yield, and seed size in the Dare population and for oleic and linoleic acid content, and height in the Tracy population. However, before adjusting for maturity, all traits showed significant location effects except for lodging and seed size in the Dare population and palmiticacid content, yield, and seed size in the Tracy population. Therefore, a good portion of the location effects were likely due to differences in planting date between locations, with Plymouth being planted nine days later than Clayton. Genotype × location was significant (P < 0.05) for all traits except stearicacid content and lodging in both populations, as well as height in the Dare population. Adjusting for maturity did not change significance of genotype × location effects in either population. For the traits that showed significant genotype × location effects, the rank correlations were relatively high (R 2 > 0.60) for all traits except yield which had a rank correlation of (R 2 < 0.38) for both populations. This indicates that significant genotype × location effects are mostly due to a change in magnitude rather than a change in rank for all traits except yield.
In hydrolysis CPO triglyceride was converted into SCPOFA (Splitted Crude Palm Fatty Acid) which had slightly higher color from the color of crude palm oil, due to high heating (250-260 o C) during hydrolysis, so that the color of impurities will be darker, but the com- position is relatively similar to CPO (Table 2). This will greatly affect the quality of the COA for DOA distillation, manufacture and purification. To manufac- ture and purify DOA lauric, myristic, palmitic (as the biggest components) and stearicacid must be sepa- rated into lower initial concentration so that the oleic acid concentration of DOA will be higher. The pro- blem is how it can be separated and what process of technology will be applied on the present facilities.
Stearicacid is a common nutritional long-chain fatty acid and is known as a potent anti-inflammatory lipid  . On the contrary, other saturated fatty acids such as myristic acid and palmiticacid are positively associated with inflammation  . Stearic is the third most abundant fatty acid in human hepatocytes  , and it is related to several liver functions, including cholesterol metabolism  and lipoprotein biogenesis  . Recent data have indicated that unlike oleic acid and linoleic acid, dietary stearicacid reduces adiposity  and inhibits cancer growth  . These effects have been attributed to a selective apoptosis impact of stearicacid on preadipocytes and cancer cells  . Dietary stearicacid increases serum oleic acid most possibly through the activation of hepatic enzymes  .
Increased long chain saturated fatty acids induce ER stress, activate the UPR and promote cell death in a great amount of cell types, such as hepatocytes  [26,27]. Thus, disruption in ER function seems lead to the pathogenesis of some diseases and to cellular impairments coupled with lipotoxicity. This was sup- ported by our observations. Previously, we found that palmiticacid causes obvious cell death in primary rat hepatocytes. To elucidate the underlying mechanism of these effects, we found that the palmiticacid causes an obvious degree of ER stress in primary rat hepatocytes. Our results demonstrated that the ER stress response contributes to palmiticacid lipotoxicity. In addition, the studies showed that a-linolenic acid protects primary rat hepatocytes against palmiticacid lipotoxicity via reducing ER stress and apoptosis. Comparing with our previous study about stearicacid, we prove that 150 μ mol/l a -linolenic acid provides very little benefits, which was presumed as the result of palmiticacid ’ s stronger ability to elicited ER stress . Furthermore, a -linolenic acid can reduce cellular dysfunction and apoptosis caused by tunicamycin. Tunicamycin, a well- known ER stress inducer, leads to apoptosis in a number of cells, including intestinal epithelial cells, renal cells and liver cells [28-30]. The mechanism on the basis of the cell necrosis induced by tunicamycin has not been clarified. These observations, together with our findings, suggest that a-linolenic acid protect primary rat hepato- cytes through alleviation of tunicamycin-induced apoptosis.
Soybeans (i.e., Glycine max L. Merr.) possessing a novel genetic determinant for the enhanced production of palmiticacid in the endogenously formed vegetableoil of the seeds are provided. Such genetic determinant is the homogeneous recessive fap5fap5 gene pair that has been found to be capable of formation through mutagenesis. Once formed, such genetic determinant can be readily transferred to other soybean lines and cultivars where it is similarly expressed on a reliable basis under conventional field growing conditions. In a preferred embodiment when a soybean plant possesses the combined presence of the homogeneous recessive genes (1) fap2-bfap2-b, (2) fap4fap4, as well as (3) fap5fap5 for enhanced palmiticacid formation in the seeds, it has been found that an unusually high expression for palmiticacid production in the resulting vegetableoil of the seeds is provided that is in excess of 30 up to approximately 37 percent by weight based upon the total fatty acid content. A resulting vegetableoil is made possible in this instance that is particularly well suited for margarine preparation in absence of the need for hydrogenation.
Abstract: The purpose of this study was to use solid lipid nanoparticles (SLN) to improve the pharmacological activity of ofloxacin. Ofloxacin-loaded SLN were prepared using palmiticacid as lipid matrix and poly vinyl alcohol (PVA) as emulsifier by a hot homogenization and ultrasonication method. The physicochemical characteristics of SLN were investigated by optical microscope, scanning electron microscopy, and photon correlation spectroscopy. Pharmacokinetics was studied after oral administration in mice. In vitro antibacterial activity and in vivo antibacterial efficacy of the SLN were investigated using minimal inhibitory concentrations (MIC) and a mouse protection model. The results demonstrated that the encapsulation efficiency, loading capacity, diameter, polydispersivity index, and zeta potential of the nanoparticles were 41.36% ± 1.50%, 4.40% ± 0.16%, 156.33 ± 7.51 nm, 0.26 ± 0.04, and −22.70 ± 1.40 mv, respectively. The SLN showed sustained release and enhanced antibacterial activity in vitro. Pharmacokinetic results demonstrated that SLN increased the bioavailability of ofloxacin by 2.27-fold, and extended the mean residence time of the drug from 10.50 to 43.44 hours. Single oral administrations of ofloxacin-loaded nanoparticles at 3 drug doses, 5 mg/kg, 10 mg/kg, and 20 mg/kg, all produced higher survival rates of lethal infected mice compared with native ofloxacin. These results indicate that SLN might be a promising delivery system to enhance the pharmacological activity of ofloxacin.
To determine the plasma epinephrine thresholds for its lipolytic effect, 60-min epinephrine infusions at nominal rates of 0.1, 0.5, 1.0, 2.5, and 5.0 micrograms/min were performed in each of four normal young adult men while they also received a simultaneous infusion of [1- 13C]palmiticacid to estimate inflow transport of plasma free fatty acids. These 20 infusions resulted in steady-state plasma epinephrine concentrations ranging from 12 to 870 pg/ml. Plasma epinephrine thresholds for changes in blood glucose, lactate, and beta-
Three months stability studies were performed for MN3 at two temperatures (5±3 and 25°C), and results are enlisted in Table 3. The MN3 suspensions stored at both temperature remains carry particles size <240 nm. PDI, zeta potential, and entrapment efficiency were Fig. 3: Differential scanning calorimetry thermogram of SAF127 copolymer, polyvinyl alcohol, pure metformin, physical mixture, and MN3 Fig. 2: Fourier transform infrared spectra of (a) SAF127 copolymer, (b) polyvinyl alcohol, (c) metformin, (d) physical mixture, and (e) MN3
Bacteriocins produced by lactic acid bacteria are pep- tides or small proteins that are frequently inhibitory to- wards many undesirable bacteria, including food-borne pathogens (e.g. Listeria monocytogenes) (L EROY et al. 2002). Bacteriocins from lactic acid bacteria can be subdivided into fourth classes. Class I of bacteriocins consists of lanthibiotics. These are small and heat-sta- ble peptides that contain thioether amino acids such as lanthionine (M ESSENS , D E V UYST 2002). Class II is divided into three sub-groups of which Class IIa is the most common. This group is composed of pediocin-like bacteriocins with anti-listerial activity. Pediocins are produced by Pediococcus spp. and while they are not very effective against spores, they are more effective
and Deshmukh et al.  both observed that increasing vegetableoil viscosity reduced the spray penetration rate, and it is suggested that this phenomenon may account for the reduction in peak heat release rate with decreasing viscosity observed in Fig. 13. Namely, it is hypothesised that in the case of all the vegetable oils a degree of fuel impingement on the piston bowl and cylinder walls is occurring and that this reduces the rate of fuel and air mixing. Therefore, where an increase in vegetableoil viscosity reduces the spray penetration rate, the incidence of fuel impingement on the piston bowl and cylinder walls will decrease also. Subse- quently, the efﬁciency of fuel and air mixing is improved (due to a reduced level of fuel impingement), and the extent of the pre- mixed burn fraction and the peak heat release rate increases. Such a hypothesis is supported by the stronger correlation of peak heat release rate at constant injection timing than at constant ignition timing (Fig. 13), as at the former condition all fuels would be sub- ject to the same initial dynamic cylinder geometry. It is also tenta- tively suggested that this may partially account for the extent of cycle to cycle variability exhibited by the sunﬂower and soybean oils (Figs. 5b and 13), as a greater degree of fuel impingement may increase the sensitivity of combustion phasing to cylinder wall heat transfer. It should however be noted that this suggested inﬂuence of vegetableoil viscosity may well vary with increasing fuel injection pressures, as several previous studies have observed increased levels of complete fuel combustion (as indicated by reduced emissions of CO and THC, and attributable to improved fuel air mixing) and also fuel spray penetration length with increasing fuel injection pressures [44–46].
The differential expression of each putative Gm FAωH was further examined in vitro using PCR based on the conditions optimized for each primer pair (Section 3.4) and equal amounts of cDNA from various soybean tissues (cv. Conrad), including root, flower, seed (M2 and L1 stages), pod (M2 and L1 stages), stem and old and young leaves. This was done with both non-DNase-treated (data not shown) and DNase-treated samples. A biological replicate was also performed using two groups of samples (‘A’ and ‘B’). All RT-PCR results were qualitatively assessed against the expression level of a housekeeping gene transcript (ACT-11). Genomic DNA was used as a positive control to show that the conditions worked with each primer and a negative control (no transcript) was also included to make sure there wasn’t any contamination or nonspecific amplification. Additionally, a control experiment was run with tissue samples generated without reverse transcriptase to ensure that any amplification that occurred in the sample was derived from the synthesized cDNA and not genomic DNA or other amplicon contamination. These are illustrated for ACT-11 (Figure 12).
Several studies have linked ER dysfunction and activa- tion of the unfolded protein response (UPR) to impair- ments in glucose homeostasis and diabetes [12,13]. ER stress and activation of the UPR in the liver have also been observed in genetic and dietary murine models of obesity, dietary models of NAFLD, and in humans with NAFLD [13-15]. A large portion of the elevated hepatic triglyceride stores in NAFLD appear to arise from re- esterification of circulating free fatty acids . Elevated circulating free fatty acids are positively correlated with liver disease severity in individuals with NAFLD . Increased non-esterified fatty acids, in particular long chain saturated fatty acids, induce ER stress and activate the UPR in a number of cell types, including hepato- cytes [15,18,19].
From the obtained calorimetric data, it is clear that the addition of 10 % CB to stearicacid was able to decrease the CI to 75 %, and 25 % CB diminished the value to less than 60 %, indicat- ing that the mixture of CB and SA was formed by a less ordered structure than pure stearicacid. A less ordered matrix favors an increasing num- ber of voids in the structure. Therefore, it is able to accommodate a larger amount of encapsulated bioactive molecules, minimizing the expulsion of these molecules during storage and enabling con- trol over their release (Muller et al., 2002). Therefore, with the use of the data obtained by WAXD and DSC for the bulk lipid mixtures, it was concluded that the addition of only 10 % CB was enough to produce significant modifications in the structure of SA, creating a new lipid matrix with more imperfections in its structure. Such a high degree of disorganization could facilitate the encapsulation of bioactive molecules and increase their retention, which is highly desirable in the matrices chosen to produce solid lipid micro/nano particles (Severino et al., 2011; Attama, Schicke, & Mueller-Goymann, 2006).
Among this last category, we noticed throughout the past years that several members of the mammalian family of membrane-bound desaturases possess a potential site of myris- toylation. Both isoforms of dihydroceramide Δ4-desaturase (DES1 and DES2) indeed present a site of myristoylation in rats (Fig. 2), mice and humans (Beauchamp et al., 2007; Mizutani et al., 2004; Ternes et al., 2002). DES1 catalyzes the last step of de novo ceramide biosynthesis which consists in the introduction of a trans Δ4-double bond in the carbon chain of the dihydroceramide. DES2 possesses a bifunctionnal Δ4-desaturase/C4-hydroxylase activity (Omae et al., 2004). The presence of the trans Δ4-double bond seems to be criti- cal for the acquisition of the biological activities of ceramide (Bielawska et al., 1993). Indeed, ceramide is able to induce apoptosis (Garcia-Ruiz et al., 1997; Gudz et al., 1997; Siskind et al., 2002), which is not the case of its precursor dihydro- ceramide. We showed that both DES1 and DES2 are myris- toylated and that this N-terminal modification significantly in- creased the activity of the recombinant DES1 when expressed in COS-7 cells (Beauchamp et al., 2007). Compared to a re- combinant unmyristoylable mutant form of DES1 (N-terminal glycine replaced by an alanine), the desaturase activity of the myristoylable wild-type DES1 was two times higher, in the presence of myristic acid incubated with the cells. The de- scription of this regulatory mechanism highlighted a new po- tential relationship between myristic acid, the saturated fatty acid capable of binding and activating the enzyme involved in the final de novo ceramide biosynthesis step, and lipoapopto- sis induced through the ceramide pathway. Indeed, we subse- quently showed that the myristoylation of recombinant DES1 can target part of the enzyme to the mitochondria, leading to an increase in ceramide levels (specifically in the mito- chondria) which in turn leads to apoptosis in the COS-7 cell model (Beauchamp, Tekpli, et al., 2009). Finally, myristic acid also increased native DES1 activity in cultured rat hepatocytes (Ezanno et al., 2012).
PA is a lipotoxic SFA that targets different organelles, including ER and mitochondria mediating hepatocyte apoptosis [6, 7]. To address the synergism between PA and MA in lipoapoptosis, we used equimolar concentrations of both fatty acids at a relevant concentration found in western diets (PA) and copra/ palmist oils (MA). Unlike PA, MA alone did not kill PMH as indicated by propidium iodide and Hoescht staining (Figure 2A). However, the combination of PA plus MA significantly increased cell death compared to PA alone (Figure 2B). As seen, the lipotoxicity of PA augmented with increasing doses of MA (Figure 2C). Moreover, while MA did not kill hepatocytes at any concentration, 0.5mM PA in the presence of MA (0.5mM) (black column Figure 2C) killed more hepatocytes than 0.5mM PA alone and similar to the degree of cell death caused by 1.0mM PA alone (light grey column Figure 2C), indicating a synergistic effect of MA in PA-induced lipotoxicity. Moreover, cell death determined by the extracellular release of glutathione-S-transferase (GST), as described in Supplemental Methods, showed similar results as those observed by propidium iodide/Hoescht staining. Further, caspase 3 activity determined by release of 7-amino- 4-trifluoromethyl coumarin from Ac-DEVD-AMC (not shown) confirmed the potentiation of PA-induced lipoapoptosis by MA. Consistent with the role of OA in increasing TG levels but not ceramide, co-incubation of PA with OA (PO) prevented cell death by PA (Figure 2B).
3.1. Cannabidiol (CBD) Prevents PalmiticAcid (PA)-Induced Drop in Mitochondrial Membrane Potential in Macrophages Palmiticacid (PA) has previously been shown to induce apoptosis of macro- phages  . Here we show that a 24 hrs incubation with palmiticacid leads to strong reduction in mitochondrial membrane potential (Figure 1; compare D-F with A-C) with concomitant shrinkage and rounding up of cells with occa- sional appearance of blebbing cells indicative for apoptosis (Figure 2; compare D-F with A-C). ImageJ analysis of red fluorescence intensity/cell shows an 80% ± 4% reduction in MitoTracker staining of PA-treated macrophages (Figure 3(A); p = 0.02). However, when the macrophages were simultaneously treated with CBD, the PA-induced drop in ∆Ψ m was significantly prevented (Figure 1;