Studies of properties and potential applications of some soluble salts of cellulose acetate phthalate. Part 1: rheological behavior and aging effect.

Rheological behaviour for solutions of the sodium, ammonium, and triethanolamie salts of cellulose acetate phthalate was studied. The comparative resistance to microbial growth and to changes in pH values exhibited by these solutions on storage was also investigated. The results indicated that the viscosities of these solutions were temperature and concentration dependent and that increasing the rate of shear produced only a slight increase of viscosity. Solutions of ammonium and the triethanolamine salts did not support any apparent microbial growth during storage at room temperature of three weeks, but the sodium salt appeared to suffer from microbial contamination. However, the use of a mixture of 0.15% methylparaben and 0.05% propylparaben prevented such contamination. The pH values of all the slat solutions studied appeared to decrease on storage.     

Investigation of some materials as dry binders for direct compression in tablet manufacture. Part 6: Effect of drug.

The effect of addition of ascorbic acid, which is a drug known to be difficult to compress directly, on the self-binding efficiency of tragacanth, Carbowax 4000, Plasdone, and mannitol were investigated. The flow properties of ascorbic acid of different particle sizes were determined since they would affect the flowability of the binders investigated and would help to determine the optimum particle size of the drug required for maximum binding efficiency.     

The effect of taurine depletion by beta-alanine treatment on the susceptibility to ethanol-induced hepatic dysfunction in rats

Alcohol was administered chronically to female Sprague-Dawley rats in a nutritionally adequate totally liquid diet for 28 days. This resulted in significant hepatic steatosis and lipid peroxidation. Beta-alanine, when co-administered with alcohol, seemed to increase hepatic steatosis, as assessed histologically, but decreased triglyceride levels as measured biochemically. In addition, beta-alanine and especially alcohol co-administered with beta-alanine, significantly increased homocysteine and cysteine excretion into urine throughout the 28-day period of ethanol administration. Serum homocysteine levels were significantly higher in alcohol- and alcohol plus beta-alanine-treated animals compared to pair-fed control animals. Alcohol did not affect the urinary excretion of taurine, except after 21 days, when levels were reduced. Levels of liver taurine were markedly depleted in animals receiving alcohol and particularly alcohol plus beta-alanine, compared to pair-fed controls. Liver and serum taurine levels were also markedly depleted in animals receiving beta-alanine and alcohol plus beta-alanine, compared to non-beta-alanine-treated animals. There was evidence of slight cholestasis in animals treated with alcohol and more so with alcohol plus beta-alanine, as indicated by raised serum alkaline phosphatase and bile acids. These in vivo findings demonstrate for the first time that animals treated with beta-alanine may be more susceptible to ethanol-induced hepatic dysfunction, possibly as a result of taurine depletion.     

Treatment of Active Crohn’s Disease With an Ordinary Food-based Diet That Replicates Exclusive Enteral Nutrition

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High-Intensity Training Reduces CD8+ T-cell Redistribution in Response to Exercise

PURPOSE: We examined whether exercise-induced lymphocytosis and lymphocytopenia are impaired with high-intensity training. METHODS: Eight trained cyclists (V˙O2max = 64.2 ± 6.5 mL·kg·min) undertook 1 wk of normal-intensity training and a second week of high-intensity training. On day 7 of each week, participants performed a cycling task, consisting of 120 min of submaximal exercise followed by a 45-min time trial. Blood was collected before, during, and after exercise. CD8 T lymphocytes (CD8TLs) were identified, as well as CD8TL subpopulations on the basis of CD45RA and CD27 expression. RESULTS: High-intensity training (18,577 ± 10,984 cells per microliter × ～165 min) was associated with a smaller exercise-induced mobilization of CD8TLs compared with normal-intensity training (28,473 ± 16,163 cells per microliter × ～165 min, P = 0.09). The response of highly cytotoxic CD8TLs (CD45RACD27) to exercise was smaller after 1 wk of high-intensity training (3144 ± 924 cells per microliter × ～165 min) compared with normal-intensity training (6417 ± 2143 cells per microliter × ～165 min, P < 0.05). High-intensity training reduced postexercise CD8TL lymphocytopenia (-436 ± 234 cells per microliter) compared with normal-intensity training (-630 ± 320 cells per microliter, P < 0.05). This was driven by a reduced egress of naive CD8TLs (CD27CD45RA). High-intensity training was associated with reduced plasma epinephrine (-37%) and cortisol (-15%) responses (P < 0.05). CONCLUSIONS: High-intensity training impaired CD8TL mobilization and egress in response to exercise. Highly cytotoxic CD8TLs were primarily responsible for the reduced mobilization of CD8TLs, which occurred in parallel with smaller neuroendocrine responses. The reduced capacity for CD8TLs to leave blood after exercise with high-intensity training was accounted for primarily by naive, and also, highly cytotoxic CD8TLs. This impaired CD8TL redistribution in athletes undertaking intensified training may imply reduced immune surveillance.     

Ratc-raf oncogene is located on chromosome 4 and may be activated by sequences from chromosome 13

Activated forms of the protooncogenec-raf have been found to transform established lines of rodent fibroblasts after transfection with DNA from several human and rat tumors. Using Southern blot analysis of DNAs from rat × mouse somatic cell hybrids, we have mappedc-raf to rat chromosome 4. An exogenous sequence that was found juxtaposed toc-raf within transforming DNA originally derived from a rat hepatocellular carcinoma was localized to chromosome 13.     

Determination of the exercise intensity that elicits maximal fat oxidation.

PURPOSE: The aim of this study was to develop a test protocol to determine the exercise intensity at which fat oxidation rate is maximal (Fat(max)). METHOD: Eighteen moderately trained cyclists performed a graded exercise test to exhaustion, with 5-min stages and 35-W increments (GE(35/5)). In addition, four to six continuous prolonged exercise tests (CE) at constant work rates, corresponding to the work rates of the GE test, were performed on separate days. The duration of each test was chosen so that all trials would result in an equal energy expenditure. Seven other subjects performed three different GE tests to exhaustion. The test protocols differed in stage duration and in increment size. Fat oxidation was measured using indirect calorimetry. RESULTS: No significant differences were found in Fat(max) determined with the GE(35/5), the average fat oxidation of the CE tests, or fat oxidation measured during the first 5 min of the CE tests (56 +/- 3, 64 +/- 3, 58 +/- 3%VO(2max), respectively). Results of the GE(35/5) protocol were used to construct an exercise intensity versus fat oxidation curve for each individual. Fat(max) was equivalent to 64 +/- 4%VO(2max) and 74 +/- 3%HR(max). The Fat(max) zone (range of intensities with fat oxidation rates within 10% of the peak rate) was located between 55 +/- 3 and 72 +/- 4%VO(2max). The contribution of fat oxidation to energy expenditure became negligible above 89 +/- 3%VO(2max) (92 +/- 1%HR(max)). When stage duration was reduced from 5 to 3 min or when increment size was reduced from 35 to 20 W, no significant differences were found in Fat(max), Fat(min), or the Fat(max) zone. CONCLUSION: It is concluded that a protocol with 3-min stages and 35-W increments in work rate can be used to determine Fat(max). Fat oxidation rates are high over a large range of intensities; however, at exercise intensities above Fat(max), fat oxidation rates drop markedly.     

The Evaluation of IL6 and ESR1 Gene Polymorphisms in Primary Dysmenorrhea

Primary dysmenorrhea is the most common gynecological complaint with painful menstrual cramps in pelvis without any pathology. It affects about half of menstruating women, and it causes significant disruption in quality of life. We investigated the association between IL6 gene promoter and ESR1 gene XbaI and PvuII polymorphisms and primary dysmenorrhea. In this case–control study, 152 unrelated young women with primary dysmenorrhea and 150 unrelated healthy age-matched controls participated. Genomic DNA was isolated and IL6 and ESR1 gene polymorphisms were genotyped using PCR-based RFLP assay. The distribution of genotype and allele frequencies of IL6 gene promoter and ESR1 gene XbaI polymorphisms were not statistically different between patients and controls (p > 0.05). However, the genotype and allele frequencies of ESR1 gene PvuII polymorphism showed statistically significant differences between primary dysmenorrhea patients and controls (p = 0.009 and p = 0.021, respectively). Statistically significant associations were also observed between age and married status of primary dysmenorrhea patients and ESR1 gene PvuII polymorphism (p = 0.044 and p = 0.023, respectively). In combined genotype analyses, AG at ESR1 XbaI and TC at ESR1 PvuII loci encoded a p-value of 0.027. Thus, individuals who are heterozygote at both loci have a lower risk of developing primary dysmenorrhea. Our study suggests no strong association between IL6 gene promoter and ESR1 gene XbaI polymorphisms and primary dysmenorrhea in Turkish women. However, ESR1 gene PvuII polymorphism showed statistically significant differences between primary dysmenorrhea patients and controls. The potential association between ESR1 gene PvuII polymorphism and age and married status of dysmenorrhea patients deserves further consideration.