Production of succinic acid from sugarcane molasses supplemented with a mixture of corn steep liquor powder and peanut meal as nitrogen sources by Actinobacillus succinogenes.

The potential of using corn steep liquor powder (CSLP), peanut meal (PM), soybean meal (SM), cotton meal (CM) and urea as the substitute of yeast extract (YE) as the nitrogen source was investigated for producing succinic acid (SA). Actinobacillus succinogenes GXAS137 was used as the fermenting bacterium and sugarcane molasses was used as the main substrate. None of these materials were able to produce SA as high as YE did. The CSLP could still be considered as a feasible and inexpensive alternate for YE as the yield of SA produced using CSLP was second only to the yield of SA obtained by YE. The use of CSLP-PM mixed formulation (CSLP to PM ratio = 2·6) as nitrogen source produced SA up to 59·2 g l(-1) with a productivity of 1·2 g l(-1) h(-1). A batch fermentation using a stirred bioreactor produced up to 60·7 g l(-1) of SA at the same formulation. Fed-batch fermentation that minimized the substrate inhibition produced 64·7 g l(-1) SA. These results suggest that sugarcane molasses supplemented with a mixture of CSLP and PM as the nitrogen source could be used to produce SA more economically using A. succinogenes. Significance and impact of the study: Succinic acid (SA) is commonly used as a platform chemical to produce a number of high value derivatives. Yeast extract (YE) is used as a nitrogen source to produce SA. The high cost of YE is currently the limiting factor for industrial production of SA. This study reports the use of a mixture of corn steep liquor powder (CSLP) and peanut meal (PM) as an inexpensive nitrogen source to substitute YE. The results showed that this CSLP-PM mixed formulation can be used as an effective and economic nitrogen source for the production of SA.

The use of konjac glucomannan hydrolysates to recover healthy microbiota in infected vaginas treated with an antifungal agent.

The aim of this study was to evaluate how konjac glucomannan hydrolysates (GMH) could support the healthy re-colonisation of vaginal microflora post infections. A total of 26 female patients (12 controls and 14 treatments) aged 18 to 25 suffering from vaginal infection were recruited for this study. Patients were assigned randomly into two groups to receive a standard antifungal treatment or a standard antifungal treatment plus pessary capsules containing 200 mg GMH (twice a week for thirty days). Patients were assessed on day zero, sixteen and thirty of the trial. Several parameters were determined including yeast and bacterial counts, the KOH test, pH, Gram staining and wet mount microscopic observations. The results showed that the counts of Candida were diminished completely with antifungal treatment for both groups. However, the total bacterial counts increased with time in the GMH pessary group unlike the control. The normalised average KOH scores were reduced sharply with time in both groups although in the control group scores started to increase after sixteen days. The normalised average white blood cell scores also decreased with time for both groups. Epithelial cell scores decreased only for the GMH pessary group while clue cells and yeast-like fungi decreased with time for both control and GMH pessary groups. These results indicate the improvement of vaginal health recovery (post antifungal treatment for Candida infection) and especially the presence of healthy microflora due to the introduction of GMH in the vagina. The data indicate that it would be worth examining further the health benefits of GMH in a vaginal health format with a view to employing the material as a prophylactic or therapeutic agent. It provides an alternative approach to reducing vaginal infections and promoting consumer health.

[Dental fluorosis of brick tea type in rats].

To observe the dental fluorosis of brick tea type, 48 white rats were fed by 245 mg.L-1 of brick tea, respectively. The rat model of brick tea type fluorosis were successfully established after 90 days. Naked eye examination of rats' incisors showed that brick tea and sodium fluoride (as positive control) groups all suffered from dental fluorosis. Using the dissecting microscope, the scanning electron microscope, and the energy spectrum apparatus, we also proved that the high concentration of brick tea could cause dental fluorosis.

Low linolenate and commercial soybean oils diminish serum HDL cholesterol in young free-living adult females.

OBJECTIVE: A mutant soybean line (A16) low in linolenic acid content (2% of oil by weight) was developed to increase oil oxidative stability. It was unknown whether serum lipid and lipoprotein concentrations in humans would be affected should A16 soybean oil (A16 oil) replace commercial soybean oil in diets. This study was conducted to examine the hypothesis that in free-living normolipidemic women, the consumption of A16 oil at approximately 10% of energy intake (en%) would not affect serum lipids and lipoproteins differently than would the consumption of the same amount of a commercial soybean oil with 7% of linolenic acid content. DESIGN: Fifteen free-living female college students consumed the soybean oil daily with regular meals for 9 weeks in different orders, with each test oil being eaten for 3 weeks. During the study, 13 en% was provided by each test oil and a total of 35 en% was from dietary fat. Serum concentrations of total cholesterol, high-density lipoprotein cholesterol (HDL cholesterol), low-density lipoprotein cholesterol (LDL cholesterol) and triacylglycerides (TAG) were measured. Serum total fatty acid patterns were analyzed as well. RESULTS: Each of the three test oils decreased serum total cholesterol, LDL cholesterol and TAG concentrations from the baseline values. The feeding of A16 and commercial soybean oils decreased serum HDL cholesterol significantly compared with coconut oil (p < 0.05). Dietary inclusion of coconut oil increased serum myristic acid significantly more than did either soybean oil (p < 0.01). Serum arachidonic acid concentrations were significantly greater with A16 consumption than with commercial soybean oil consumption (p < 0.001). CONCLUSION: A16 and commercial soybean oils both diminished serum HDL cholesterol. Although the fatty acid composition differed between the two soybean oils, A16 oil and commercial oil had similar effects on serum concentrations of lipoproteins and lipids. With increased oxidative stability, A16 oil is a good alternative to commercial soybean oil.

Experimental study using a direct current electrical field to promote peripheral nerve regeneration.

A direct current (DC) electrical field was used to stimulate transected and sutured rat sciatic nerve. Electrophysiologic, morphometric, and functional assessments were carried out on days 10, 20, 30, and 60 postoperatively. The results showed that the electrophysiologic index, the diameter and myelin-sheath thickness of regenerating nerve fibers, the sciatic functional index (SFI), and the strength of the triceps surae muscle in the experimental group were much better than those in the control group. This indicated that DC electrical stimulation could effectively promote peripheral nerve regeneration and produce positive effects after 3 weeks, and that the stimulator was not rejected by the host for a relatively long period of time.

[Protective effects of gypenosides on experimental myocardial infarction].

In the model of myocardial infarction produced by occlusion of left anterior descending coronary artery (LAD) in rabbit, gypenosides (GP 100 but not 50 mg/kg, ip) reduced myocardial infarct size and decreased serum free fatty acid (FFA). In rat model of myocardial infarction, GP and the fractions of GP of non ginsenosides (FGNG) both in dose of 100 mg/kg, ip, protected significantly myocardial superoxide dismutase (SOD) activity and decreased the myocardial malondialdehyde (MDA). The results indicate that the protective effect of GP on myocardial infarction may be correlated with its prevention of myocardial lipid peroxidation, and attributed to the amelioration of FFA metabolic deterioration.